Case Report of a 63-Year-Old Patient With Alzheimer Disease and a Novel Presenilin 2 Mutation : Alzheimer Disease & Associated Disorders
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Case Report of a 63-Year-Old Patient With Alzheimer Disease and a Novel Presenilin 2 Mutation
Wells, Jennie L. BSc, MSc, MD, FACP, FRCPC, CCRP *,† ; Pasternak, Stephen H. MD, PhD, FRCPC †,‡,§
* Department of Medicine, Division of Geriatric Medicine, Schulich School of Medicine and Dentistry, Western University
† St. Joseph’s Health Care London—Parkwood Institute
‡ Molecular Medicine Research Group, Robarts Research Institute
§ Department of Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada
The authors declare no conflicts of interest.
Reprints: Jennie L. Wells, BSc, MSc, MD, FACP, FRCPC, CCRP, Department of Medicine, Division of Geriatric Medicine, St. Joseph’s Health Care London—Parkwood Institute, Room A2-129, P.O. Box 5777 STN B, London, ON, Canada N6A 4V2 (e-mail: [email protected] ).
This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0/
Early onset Alzheimer disease (EOAD) is a neurodegenerative dementing disorder that is relatively rare (<1% of all Alzheimer cases). Various genetic mutations of the presenilin 1 ( PSEN1 ) and presenilin 2 ( PSEN2 ) as well as the amyloid precursor protein (APP) gene have been implicated. Mutations of PSEN1 and PSEN2 alter γ-secretase enzyme that cleaves APP resulting in increase in the relative amount of the more amyloidogenic Aβ42 that is produced. 1
PSEN2 has been less studied than PSEN1 and fewer mutations are known. Here, we report a case of a 63-year-old woman (at the time of death) with the clinical history consistent with Alzheimer D, an autopsy with brain histopathology supporting Alzheimer disease (AD), congophylic angiopathy, and Lewy Body pathology, and whose medical genetic testing reveals a novel PSEN2 mutation of adenosine replacing cytosine at codon 222, nucleotide position 665 (lysine replacing threonine) that has never been previously reported. This suggests that genetic testing may be useful in older patients with mixed pathology.
CASE REPORT
The patient was referred to our specialty memory clinic at the age of 58 with a 2-year history of repetitiveness, memory loss, and executive function loss. Magnetic resonance imaging scan at age 58 revealed mild generalized cortical atrophy. She is white with 2 years of postsecondary education. Retirement at age 48 from employment as a manager in telecommunications company was because family finances allowed and not because of cognitive challenges with work. Progressive cognitive decline was evident by the report of deficits in instrumental activities of daily living performance over the past 9 months before her initial consultation in the memory clinic. Word finding and literacy skills were noted to have deteriorated in the preceding 6 months according to her spouse. Examples of functional losses were being slower in processing and carrying out instructions, not knowing how to turn off the stove, and becoming unable to assist in boat docking which was the couple’s pastime. She stopped driving a motor vehicle about 6 months before her memory clinic consultation. Her past medical history was relevant for hypercholesterolemia and vitamin D deficiency. She had no surgical history. She had no history of smoking, alcohol, or other drug misuse. Laboratory screening was normal. There was no first-degree family history of presenile dementia. Neurocognitive assessment at the first clinic visit revealed a Mini Mental State Examination (MMSE) score of 14/30; poor verbal fluency (patient was able to produce only 5 animal names and 1 F-word in 1 min) as well as poor visuospatial and executive skills ( Fig. 1 ). She had fluent speech without semantic deficits. Her neurological examination was pertinent for normal muscle tone and power, mild ideomotor apraxia on performing commands for motor tasks with no suggestion of cerebellar dysfunction, normal gait, no frontal release signs. Her speech was fluent with obvious word finding difficulties but with no phonemic or semantic paraphrasic errors. Her general physical examination was unremarkable without evidence of presenile cataracts. She had normal hearing. There was no evidence of depression or psychotic symptoms.
At the time of the initial assessment, her mother was deceased at age 79 after a hip fracture with a history long-term smoking and idiopathic pulmonary fibrosis. Her family believes that there is possible German and Danish descent on her father’s side. Her father was alive and well at age 80 at the time of her presentation with a history coronary artery disease. He is still alive and well with no functional or cognitive concerns at age 87 at the time of writing this report. Her paternal grandfather died at approximately age 33 of appendicitis with her paternal grandmother living with mild memory loss but without known dementia or motor symptoms until age 76, dying after complications of abdominal surgery. Her paternal uncle was diagnosed with Parkinson disease in his 40s and died at age 58. Her maternal grandmother was reported to be functionally intact, but mildly forgetful at the time of her death at age 89. The maternal grandfather had multiple myocardial infarctions and died of congestive heart failure at age 75. She was the eldest of 4 siblings (ages 44 to 56 at the time of presentation); none had cognitive problems. She had no children.
Because of her young age and clinical presentation with no personality changes, language or motor change, nor fluctuations, EOAD was the most likely clinical diagnosis. As visuospatial challenges were marked at her first visit and poor depth perception developing over time, posterior cortical variant of AD was also on the differential as was atypical presentation of frontotemporal dementias. Without fluctuations, Parkinsonism, falls, hallucinations, or altered attention, Lewy Body dementia was deemed unlikely. After treatment with a cholinesterase inhibitor, her MMSE improved to 18/30, tested 15 months later with stability in function. Verbal fluency improved marginally with 7 animals and 3 F-words. After an additional 18 months, function and cognition declined (MMSE=13/30) so memantine was added. The stabilizing response to the cholinesterase inhibitor added some degree of confidence to the EOAD diagnosis. In the subsequent 4 years, she continued to decline in cognition and function such that admission to a care facility was required with associated total dependence for basic activities of daily living. Noted by family before transfer to the long-term care facility were episodic possible hallucinations. It was challenging to know if what was described was misinterpretation of objects in view or a true hallucination. During this time, she developed muscle rigidity, motor apraxias, worsening perceptual, and language skills and became dependent for all activities of daily livings. At the fourth year of treatment, occasional myoclonus was noted. She was a 1 person assist for walking because of increased risk of falls. After 1 year in the care home, she was admitted to the acute care hospital in respiratory distress. CT brain imaging during that admission revealed marked generalized global cortical atrophy and marked hippocampal atrophy ( Fig. 2 ). She died at age 63 of pneumonia. An autopsy was performed confirming the cause of death and her diagnosis of AD, showing numerous plaques and tangles with congophilic amyloid angiopathy. In addition, there was prominent Lewy Body pathology noted in the amygdala.
Three years before her death informed consent was obtained from the patient and family to perform medical genetic testing for EOAD. The standard panel offered by the laboratory was selected and included PSEN1 , PSEN2 , APP, and apoE analysis. Tests related to genes related to frontotemporal dementia were not requested based on clinical presentation and clinical judgement. This was carried out with blood samples and not cerebrospinal fluid because of patient, family, and health provider preference. The results revealed a novel PSEN2 mutation with an adenosine replacing cytosine at nucleotide position 665, codon 222 [amino acid substation of lysine for threonine at position 221 (L221T)]. This PSEN2 variant was noted to be novel to the laboratory’s database, noting that models predicted that this variant is likely pathogenic. The other notable potentially significant genetic finding is the apoliprotein E genotype was Є 3/4 .
β-amyloid (Aβ) is a 38 to 43 amino acid peptide that aggregates in AD forming toxic soluble oligomers and insoluble amyloid fibrils which form plaques. Aβ is produced by the cleavage of the APP first by an α-secretase, which produces a 99 amino acid C-terminal fragment of APP, and then at a variable “gamma” position by the γ-secretase which releases the Aβ peptide itself. It is this second γ-cleavage which determines the length and therefore the pathogenicity of the Aβ peptides, with 42 amino acid form of Aβ having a high propensity to aggregate and being more toxic.
The γ-secretase is composed of at least 4 proteins, mAph1, PEN2, nicastrin, and presenilin . Of these proteins, presenilin has 2 distinct isoforms ( PSEN1 and PSEN2 ), which contain the catalytic site responsible for the γ-cleavage. PSEN mutants are the most common genetic cause of AD with 247 mutations described in PSEN1 and 48 mutations described in PSEN2 (Alzgene database; www.alzforum.org/mutations ). PSEN2 mutations are reported to be associated with AD of both early onset and variable age onset as well as with other neurodegenerative disorders such as Lewy Body dementia, frontotemporal dementia, Parkinson dementia, and posterior cortical atrophy. 2–4 In addition, PSEN2 has associations with breast cancer and dilated cardiomyopathy. 3
PSEN2 mutants are believed to alter the γ-secretase cleavage of APP increasing the relative amount of the more toxic Aβ42. The mean age of onset in PSEN2 mutations, is 55.3 years but the range of onset is surprisingly wide, spanning 39 to 83 years. Over 52% of cases are over 60 years. All cases have extensive amyloid plaque and neurofibrillary tangles, and many have extensive alpha-synuclein pathology as well. 5
In considering the novelty of this reported PSEN2 mutation , a literature search of Medline, the Alzgene genetic database of PSEN2 and the Alzheimer Disease and Frontotemporal Dementia Mutation Databases (AD&FTMD) were completed ( www.molgen.vib-ua.be/ADMutations ). The mutation presented here (L221T) has never been described before.
Although this mutation has not been described, we believe that it is highly likely to be pathogenic. This mutation is not conservative, as it replaces a lysine residue which is positively charged with threonine which is an uncharged polar, hydrophilic amino acid. The mutation itself occurs in a small cytoplasmic loop between transmembrane domain 4 and 5, which is conserved in the PSEN1 gene, and in PSEN2 is highly conserved across vertebrates, including birds and zebrafish all the way to Caenorhabditis elegans , but differs in Drosophila melanogaster (fruit fly) ( Fig. 3 ). We examined this mutation using several computer algorithms which examine the likelihood that a mutation will not be tolerated. Both SIFT ( http://sift.bii.a-star.edu.sg ) and PolyPhen-2.2.2 (HumVar) ( www.bork.embl-heidelberg.de/PolyPhen ) predicts that this variant is pathogenic. Interestingly, it is noted that PSEN1 mutations after amino acid 200 develop amyloid angiopathy. 5,7
This patient also had an additional risk factor for AD, being a heterozygote for the apoЄ4 allele. Among other mechanisms, its presence reduces clearance of Aβ42 from the brain and increases glial activation. 8 Although the apoЄ4 allele is known to lower the age of onset of dementia in late onset AD, it has not been clearly shown to influence age of onset of EOAD in a limited case series. 9 It should be noted that heterozygote state may have contributed to an acceleration of her course given the known metabolism of apoЄ4 and its association with accelerated cerebral amyloid and known reduction in age of onset. 10
Given that there is no definite family history of autosomal dominant early onset dementia, it is likely that her PSEN2 mutation was a new random event. With the unusually wide age of onset it is conceivable that one of her parents could still harbor this PSEN2 mutation . The patient’s father, however, is currently 87 and living independently at the time of writing this manuscript, making him highly unlikely to be an EOAD carrier. Nonpaternity is an alternate explanation for the lack of known first-degree relative with EOAD; however, this is deemed unlikely by the family member who provided the supplemental history. Her mother died at age 79, so she could conceivably carry our mutation but we do not have access to this genetic material. Without extensive testing of many family members it would be impossible to speculate about autosomal recessive form of gene expression. In addition, the genetic testing requested was limited to presenilins , APP, and apoE mutations. Danish heritage may add Familial Danish dementia as a remote consideration; however, Familial Danish dementia has a much different clinical presentation with long tract signs, cerebellar dysfunction, onset in the fourth decade as well as hearing loss and cataracts at a young age. 11 This disease has high autosomal dominant penetration which also makes it less likely in the patient’s context. This specific gene (chromosome 13) was not tested. The autopsy findings do not support this possibility. There are reports of Familial AD pedigrees in Germany, including a Volga pedigree with PSEN141I mutation in exon 5, but this is clearly separate from our mutation which is in exon 7. Our mutation was also not observed in a recent cohort of 23 German individuals with EOAD which underwent whole genome sequencing, but did find 2 carriers of the Volga pedigree. It is also possible that both the PSEN2 mutation and the ApoE genotype contributed to her disease and early onset presentation. This case illustrates the multiple pathology types which occur in individuals bearing PSEN2 mutations, and highlights the later ages in which patients can present with PSEN2 mutations. 12
ACKNOWLEDGMENT
The authors acknowledge Gwyneth Duhn, RN, BNSc, MSc, for her support of this paper.
Alzheimer disease; presenilin ; mutation
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- Case of early-onset Alzheimer’s disease with atypical manifestation
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- http://orcid.org/0000-0003-1224-4320 Lin Zhu 1 ,
- Limin Sun 2 ,
- Lin Sun 3 , 4 and
- Shifu Xiao 3 , 4
- 1 Department of Rehabilitation Medicine , Shanghai No.3 Rehabilitation Hospital , Shanghai , China
- 2 Department of Rehabilitation Medicine , Huashan Hospital Fudan University , Shanghai , China
- 3 Department of Geriatric Psychiatry , Shanghai Mental Health Center , Shanghai , China
- 4 Alzheimer's Disease and Related Disorders Center, Shanghai Jiao Tong University , Shanghai , China
- Correspondence to Professor Shifu Xiao; xiaoshifu{at}msn.com
Short-term memory decline is the typical clinical manifestation of Alzheimer’s disease (AD). However, early-onset AD usually has atypical symptoms and may get misdiagnosed. In the present case study, we reported a patient who experienced symptoms of memory loss with progressive non-fluent aphasia accompanied by gradual social withdrawal. He did not meet the diagnostic criteria of AD based on the clinical manifestation and brain MRI. However, his cerebrospinal fluid examination showed a decreased level of beta-amyloid 42, and increased total tau and phosphorylated tau. Massive amyloid β-protein deposition by 11C-Pittsburgh positron emission tomography confirmed the diagnosis of frontal variant AD. This case indicated that early-onset AD may have progressive non-fluent aphasia as the core manifestation. The combination of individual and precision diagnosis would be beneficial for similar cases.
- dual (psychiatry)
- cognition disorders
This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ .
http://dx.doi.org/10.1136/gpsych-2020-100283
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Introduction
Clinical report and methods.
Early-onset Alzheimer’s disease (EOAD), which comprises 5% of Alzheimer’s disease (AD), shows a 1.6-year average delay in diagnosis compared with late-onset AD. 1 2 The clinical phenotype of atypical EOAD is heterogeneous, and primary progressive aphasia (PPA) is rarely the initial manifestation of related dementia syndromes. Compared with the progressive non-fluent aphasia (PNFA) related to the language variant phenotype of frontotemporal lobar degeneration (FTLD), molecular imaging studies in patients with primary progressive aphasia suggest the pathological basis of AD. 3 Neurodegeneration uaually starts in a specific neural anatomic networks. The clinical phenotype of PPA can usually infer the type of protein degeneration, which can be used to infer gene mutation. With the development of biomarkers such as genetics, molecular biology, neuroimaging and positron emission tomography (PET), accurate diagnosis can be gradually achieved. In this case study, we describe an AD patient with PNFA as the first symptom.
The patient was a 63-year-old married man, a right-handed businessman, native of Shanghai, with 12 years of school education. He has memory loss and non-fluent speech for 7 years combined with personality changes for 5 years. The patient recovered from hepatitis A 32 years ago and has well-controlled hypertension for 30 years.
The patient’s caregiver described that the patient showed forgetfulness and developed poor pronunciation at the age of 56. His short-term memory has gradually declined as noticed that he repeatedly gave money to customers while selling clothes. He frequently forgot where he parked his bicycle, and it was hard for him to speak a full sentence; his language was vague and short. He was impatient when being asked to repeat a word. Over time, he could only say some single syllables. He evolved into fully aphasia gradually, and his personality also changed gradually. At the age of 59, he could not recognise himself in the mirror and he often hid his shoes because he was worried that they would be stolen. Therefore, his wife had accompanied him to see a neurologist. The physical and neurological examination revealed no remarkable signs. His brain MRI showed mild atrophy in the bilateral frontal lobe ( figure 1A at the age of 59). Fluorodeoxyglucose positron emission tomography (FDG-PET) revealed that glucose metabolism in the bilateral frontal and parietal lobe was declined, and the left side was significant ( figure 1B at the age of 59). The Mini-Mental State Examination (MMSE) score was 18 out of 30 (18/30). At that point, he was diagnosed with cognitive impairment and treated with rivastigmine. After the treatment, his memory improved slightly. In 2017, the neurologist gave him quetiapine and donepezil due to developing visual hallucinations and irritability. The second brain MRI scan revealed increased frontal and temporal atrophy compared with the first one ( figure 1C at the age of 61). The FDG-PET revealed that the cerebral cortical glucose metabolism was further reduced, especially the bilateral frontal and parietal lobes were obvious ( figure 1D at the age of 61).
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Brain imaging and cognitive score of the patient. (A) The patient’s MRI in May 2015 revealed mild atrophy of the bilateral frontal lobe (at the age of 59). (B) The patient’s FDG-PET in May 2015 revealed that glucose metabolism in the bilateral frontal and parietal lobe was reduced, and the left side was significant (at the age of 59). (C) The patient’s MRI in July 2017 (2 years after the first scan), revealed more atrophy of the bilateral frontal lobe and temporal lobe atrophy occurred (at the age of 61). (D) The patient’s FDG-PET in August 2017 revealed that the cerebral cortical glucose metabolism was reduced more, bilateral frontal and parietal lobes obvious in particular (at the age of 61). (E) The patient’s third MRI in May 2019 (2 years after the second scan) revealed atrophy of the whole cerebral cortex with bilateral frontal lobes, temporal lobe and hippocampus more affected (at the age of 63). (F) The patient’s 11C-PIB PET in May 2019 revealed saliently amyloid deposition in diffuse cortical areas, particularly in the bilateral frontal, parietal, temporal cortices and posterior cingulated gyrus (at the age of 63). (G) Mini-Mental State Examination (MMSE) of the patient. MMSE in May 2015 revealed a total score was 18/30 (at the age of 59). MMSE in May and December 2019 revealed a total score were 3/30 and 2/30; the results showed severe impairments in language and other cognitive areas (at the age of 63). 11C-PIB PET, 11C-Pittsburgh compound B positron emission tomography; FDG-PET, fluorodeoxyglucose positron emission tomography.
In May 2019, the patient’s symptoms aggravated further, which included bad temper, crying often and being more difficult to be looked after. His wife brought him to seek help from a psychiatrist, and he was admitted into the Department of Geriatric Psychiatry of Shanghai Mental Health Center. He underwent routine laboratory tests to exclude non-neurodegenerative and dementia. His neurological examination showed gait abnormality, negative Babinski’s sign, muscular tension hyperactivity, knee jerk reflex hyperactivity and a weak positive right palmar jaw reflex. The MMSE score was 3/30. The patient exhibited severe impairments in orientation (2/10), attention and calculation (1/5), recall (0/6), language (0/8) and visual construction (0/1). The Montreal Cognitive Assessment score was 0 (0/30), which was significantly lower than it was in 2015( figure 1G ). The third brain MRI demonstrated atrophy of the cerebral cortex, especially in the bilateral frontal lobes and hippocampus. The medial temporal lobe atrophy scale was at grade 3 ( figure 1E at the age of 63).
In addition, we tested three pathogenic genes for early-onset AD including amyloid precursor protein, presenilin-1, presenilin-2 genes related to neurocognitive disorders, but no mutation was found. Apolipoprotein E (APOE) genotyping showed APOE ε3/ε3 type. In order to reach a definite diagnosis, the patient underwent 11C-Pittsburgh compound B positron emission tomography (11C-PIB PET) and cerebrospinal fluid (CSF) examination. 11C-PIB PET revealed noticeable amyloid deposition in diffuse cortical areas, particularly in the bilateral frontal, parietal, temporal cortices and posterior cingulated gyrus ( figure 1F at the age of 63). The measured CSF biomarkers showed decreased amyloid β-protein (Aβ) 42 (462 pg/ml; cut-off >562 pg/ml), increased total tau (754 pg/ml; cut-off <370 pg/ml) and increased phosphorylated tau (87.40 pg/ml; cut-off <66.26 pg/ml). Eventually, the diagnosis of frontal variant EOAD was reconfirmed considering the early onset of dementia, the slow progression of symptoms, the absence of focal neurological damage signs and the exclusion of other systemic or brain diseases that could cause dementia. Due to the gastrointestinal adverse reactions of the patient, rivastigmine was suspended. We used memantine 10 mg b.i.d. and donepezil 5 mg q.d. to improve cognition and to control psychobehavioural symptoms and vortioxetine 10 mg q.d. to improve mood. After the treatment and follow-up for 7 months, the patient’s behaviour and mood was improvved significally, and his language expression improved slightly ( figure 1G at the age of 63).
The initial clinical manifestations of the patient included short-term memory decline, poor pronunciation and personality changes at an early stage, followed by behavioural and psychological symptoms of dementia, including hallucinations, delusions of theft, gradual decline in self-care as well as depression. The patient’s brain MRI initially showed mild atrophy of the bilateral frontal lobe. With the progress of the disease, more severe atrophy of the cerebral cortex, temporal lobe and hippocampus appeared besides the further atrophy of the bilateral frontal lobe. The atypical manifestation such as early aphasia, frontal lobe atrophy and personality changes can mislead clinicians in diagnosing frontotemporal lobar degeneration. This is the main reason leading to the misdiagnosis of this patient, which should be taken as a lesson or future reference for clinicians.
According to the current classification schemes, the clinical symptoms were in line with PNFA, which are halting speech by speech sound errors with spared content word comprehension and atrophy of the left frontal lobe. 4 PNFA is one of the primary progressive aphasias. 4 This patient met the diagnostic criteria of frontotemporal dementia, consistent with the early personality changes and cognitive abnormalities. 5 In the past 7 years, the patient’s speech fluency and cognitive function decreased continuously and rapidly. The clinical manifestations could not be explained by typical AD. The CSF phosphorylated tau was slightly higher, and no gene mutations associated with AD were found, which further made it harder to reach the diagnosis. However, the 11C-PIB PET showed heavy and extensive Aβ-amyloid depositions and provided definite pathological evidence of AD. A retrospective study found PNFA with 13%– 31% of cases might have the pathology of AD. 6 The patient met the research diagnostic AT(N) framework of AD, with A: (11C-PIB PET revealed amyloid depositions, CSF Aβ42 decreased), T: (CSF phosphorylated microtubule-associated protein tau increased) and N: (cortical atrophy on MRI, glucose hypometabolism in the bilateral frontal parietal lobe and CSF total microtubule-associated protein tau increased). 7 We use the AD pathological markers as the gold standard to exclude other types of dementia and reach an earlier and more accurate diagnosis. It’s worth pointing out that the patient might have mixed neuropathology. Santos-Santos 6 found that 75% of PNFA or PPA cases may have mixed pathological changes of FTLD and AD. This poses a new challenge for clinicians, suggesting that verified, reliable and accessible biomarkers for diagnosis of FTLD should be developed urgently. Otherwise, the comorbid pathological cases would only be accurately diagnosed after autopsy.
After reaching a clear diagnosis, and according to the China guidelines for the diagnosis and treatment of dementia and cognitive impairment in 2018 and the guidelines for the diagnosis and treatment of AD, 8 the patient was treated with cholinesterase inhibitors and excitatory amino acid receptor antagonists to enhance cognition, and antidepressants were given to relieve his mood. After the treatment, the patient’s symptoms were improved, and his mood was stable. Additionally, the biopsychosocial medical model has become more and more accepted. We should treat the patients with medication and non-drug intervention for patients and their caregivers. Spouses and caregivers of patients with early-onset dementia bear a greater burden and higher depression rates. 9 The speech impairments of this patient appeared early. He was emotionally unstable, grumpy and easy to be tearful, which was alleviated when his wife comforted him. Two weeks later, he was released from the hospital and continued to receive comprehensive rehabilitation treatments. Anyway, providing individualised psychosocial support for patients and their caregivers is very important for improving symptoms and quality of life. 10
Some of PNFAs are due to the underlying pathology of AD, which is more common in EOAD. In the present case, neither clinical examination nor MRI could definitively differentiate FTLD from EOAD. According to AT(N) research framework, we could eventually confirm the neuropathy diagnosis of AD or frontal-variant AD (fvAD), but the previous misdiagnoses were significant. FvAD can lead to social withdrawal and depression. These patients should benefit from accurate diagnosis, medication treatment and individualised psychosocial intervention.
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Lin Zhu obtained a bachelor’s degree in clinical medicine from Shanghai Jiao Tong University School of Medicine, Shanghai, China in 2006. She is currently working as an attending doctor and psychotherapist at the Neurorehabilitation Department of Shanghai Third Rehabilitation Hospital. After completing clinical training, she started a two-year master program and was certified by the Institute of Psychology of the Chinese Academy of Sciences. In addition, she has also been trained and actively involved in clinical neurological research for half year in the Department of Geriatric Psychiatry of Shanghai Mental Health Center, Shanghai, China. Her main research interest includes the rehabilitation of elderly with psychiatric disorders.
Contributors LZ drafted the case report and manuscript; LMS performed the literature search; LS and SX supervised and revised the manuscript. All authors approved the final manuscript.
Funding This study was supported by a grant of Clinical Research Centre Project of Shanghai Mental Health Centre (CRC2017ZD02) and Scientific Research Program of Shanghai Jing an District Health Committee (2020MS16).
Competing interests None declared.
Patient consent for publication Parental/guardian consent obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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An Alzheimer Disease Case Study
Cleveland Clinic Lou Ruvo Center for Brain Health in Las Vegas provides treatment options for Alzheimer’s disease patients and support for their caregivers.
An initial conversation with Harvey and Jane Levy reveals little about the fact that Mr. Levy, 71, is battling Alzheimer disease. Both husband and wife have a good sense of humor and an obvious love of life. After nearly 50 years together, Mr. Levy’s diagnosis is one of the biggest challenges they’ve had to face. When Mr. Levy, a retired electrical contractor in Los Angeles, was diagnosed five years ago, they turned to Cleveland Clinic Lou Ruvo Center for Brain Health in Las Vegas.
Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services Policy
“The disease affects everybody differently. With Harvey, it’s unfortunately his speech,” says Mrs. Levy. “He knows what he wants to say, but he can’t always get it out.”
Paving the way for new treatments
Today, numerous clinical trials are underway to help patients like Mr. Levy. He is currently participating in the NOBLE study at the Lou Ruvo Center for Brain Health, coordinated by the Alzheimer’s Disease Cooperative Study . This study is evaluating an investigational oral drug for patients with mild to moderate Alzheimer disease. The study includes 450 patients at research sites across the country. Total participation time is about 14 months, during which Mr. Levy is being carefully monitored. Studies have shown that this investigational drug may work by protecting brain cells, which could result in slowing the progress of the memory loss.
Clinical research coordinator Yolande Mucharbach at the Lou Ruvo Center for Brain Health says clinicians speak with patients and caregivers about clinical trials and encourage them to think about participating if they are eligible.
“It’s people like Harvey and Jane Levy and others in the study who are paving the way to find a new treatment for Alzheimer disease,” she says.
Caregiver support
At the Lou Ruvo Center for Brain Health, there are weekly caregiver support groups available to help family members of individuals with Alzheimer disease in dealing with the significant changes their loved ones face. Led by a psychologist, the meetings are confidential, free and open to the community. Meetings are structured so members can share their experiences with others and exchange ideas and resources for coping with challenging situations that may arise in their role as care partners.
Mrs. Levy says the group meetings provide a safe and nonjudgmental place. Thanks to the group, she says she has made friends with other people who understand what she’s going through.
“We met this fabulous couple, and we go out with them all the time,” she says. “Her husband has trouble with short-term memory, and Harvey has trouble with speech, but we get along great.”
Mrs. Levy also has weekly lunch date with some of the women from the group.
Other programs and classes at the center are designed to keep patients engaged in life. For the past year, the Levys have been attending an art class where they learn about various pieces of art. Now, they’re signed up for another art class in which they’ll be creating the art.
“Cleveland Clinic has been a godsend for us on so many levels,” Mrs. Levy says. “The support, the interaction and the hope that it might actually work make it well worth it.”
And Mrs. Levy goes on to say that she and Mr. Levy have three sons who could potentially inherit the disease. The couple wants to do everything it can to further research and help others.
Learn more about AD clinical trials .
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Early-Onset Alzheimer's: A Case Study
- 2 Introduction
- 3 Client Characteristics
- 4.1 Subjective
- 4.2 Objective
- 5.1 Problem List
- 6.1 Patient Goals
- 6.2 Treatment Plan
- 8 Discussion
- 9 References
Abstract [ edit | edit source ]
Alzheimer's is the most common cause of dementia . It is characterized by a gradual degradation of various physical and cognitive functions [1] . The current fictional case study is about a 42 year old female with early onset Alzheimer’s Disease (EOAD) seeking physiotherapy treatment. Evaluation findings include gait abnormalities, decreased balance and decreased cognition. She presented with forward head posture with slight postural kyphosis and palpable muscle tightness in upper trapezius. Slight weakness in lower extremities (L/E), and decreased shoulder flexion bilaterally. The physiotherapy intervention component includes education, home based exercise programs addressing aerobic and strengthening deficits. Following the physiotherapy intervention, Mrs. S improved her AROM, muscular strength, postural control and gait all the while decreasing overall fatigue and risk of falls. Throughout the treatment plan there were no changes in cognitive function. Mrs. S will continue to be involved in interprofessional care to maintain her quality of life. The physiotherapist’s role in EOAD cases is to maximize independence to help prevent the progression of physical and cognitive decline [2] . In the future, more research must be conducted to determine the adequate frequency, intensity, and duration of treatment for patients with EOAD [3] [4] .
Introduction [ edit | edit source ]
Alzheimer's is “a type of dementia that causes problems with memory, thinking and behaviour. Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks” [1] . Literature shows that physical activity has been repeatedly found to improve the ability of patients with dementia to perform activities of daily living (ADLs) [5] . However, it seems that the frequency, intensity, and duration of exercises prescribed in order to elicit benefits varies widely between studies [5] . On the other hand, research regarding the effects of physical activity on the cognitive function of patients with dementia are inconclusive. A review conducted by McDonnell et al., stated that there is a small effect of aerobic exercise programs on improving cognitive function [6] . However, another review states that an exercise program combining aerobic and strength conditioning evokes no effects on cognitive function [7] . The current case study describes a patient with EOAD who presents with mild difficulties with her ADLs as well as other symptoms such as reduced balance, gait abnormalities, reduced aerobic capacity, and cognitive decline. This report strives to document the changes in the patient’s symptom presentation throughout her involvement in physiotherapy.
Client Characteristics [ edit | edit source ]
Mrs. S, a 42 year old female with a 1 year history of EOAD presents to the clinic. She previously worked as a full-time administrator at a real estate office. She is recently unemployed due to the worsening of her condition in the last 3 months. Various progressive cognitive symptoms such as memory deficits and confusion have rendered her unfit to continue to work. Mrs. S sought for physiotherapy in order to delay the physical progression of the disease. Her chief complaints include mild difficulties with gait, balance, and being fatigued easily. She noted that she has stumbled and tripped several times in the past 3 months but was fortunately not hurt. She has also noticed the increasing difficulty she is having with fine motor skills such as writing and doing up her buttons when dressing. With the diagnosis of EOAD, the patient is at an increased risk of various secondary conditions such as osteoporosis and falls.
Examination Findings [ edit | edit source ]
Subjective [ edit | edit source ].
- Patient Profile (PP): 42 y/o female
- History of Present Illness (HPI): Diagnosed with EOAD 1 year ago, presenting with mild cognitive and physical deficits, not currently receiving treatment interventions from PT.
- Past medical history: Depression
- Medications: Celexa (citalopram) 20mg/day, donepezil (aricept) 10mg/day
- Health Habits: Non-smoker, 1 glass of red wine per week, no other substances
- Family History: Mother passed away from complications of EOAD in 2001
- Social History: Recently resigned from full time position as administrator at a real estate office due to cognitive difficulties. Lives alone in a bungalow with her pet dog. Family lives in the next town over (25 minute drive). Currently spends majority of her day walking her dog and babysitting her neighbours’ kids. Imaging: Magnetic resonance imaging (MRI), Positron Emission Tomography (PET), Single-Photon Emission Computed Tomography (SPECT)
Precautions/Contraindications: Slight confusion with short term memory, risk of agitation, current unemployment, and depression.
Objective [ edit | edit source ]
Vitals: HR: 80 bpm, BP: 120/80 mmHg, RR= 20 bpm.
Observation: Forward head posture (protracted) along with slight increased postural kyphosis. Palpable muscle tightness in upper trapezius. Patient appears to be slightly deconditioned.
- Cervical AROM= slightly limited in extension
- Shoulder AROM= bilateral shoulder flexion decreased.
- All other UE AROM= WNL
- U/E sensation intact
- L/E AROM= limited trunk extension, all other WNL
- L/E sensation intact
Isometric break test (IBT) :
- Upper extremities: strong, pain free, and good motor control.
- Lower extremities: slightly weak, pain free, and good motor control.
Coordination Tests:
- Finger to nose: smooth and controlled, with slight dysmetria bilaterally
- Finger opposition: mild bilateral impairment in coordination
Self-reported outcome measures:
- Functional Activities Questionnaire (FAQ): Score of 13/30
- Generalized Anxiety Disorder (GAD-7): 8/21
- Patient Health Questionnaire (PHQ-9): 10/27
Outcome measures:
- Mini-mental State Examination ( Mental Health Outcome Measures for Physiotherapists in Clinical Practice ): score of 20/30
- Clock drawing test: score of 2/5 on the Shulman Method
- Timed Up and Go Test (TUG) : 13 seconds
- Mini- Balance Evaluation Systems Test (BESTest) : Score of 21/28.
Clinical Impression [ edit | edit source ]
Major clinical findings identified during the subjective interview were the patient’s history of falls, gait abnormalities, and decreased cognition due to the progression of her condition. This is affecting her ADLs, sleep quality and quantity, as well as her interaction with others. She was no longer able to work due to cognitive and physical changes. These factors, in combination with her condition, appear to be negatively impacting her functionality which was once at a high level prior to her diagnosis. This is reflected in her FAQ score of 13/30 indicating impaired function and possible cognitive impairment [8] . Both her GAD-7 score of 8/21 and her PHQ-9 score of 10/27 reflect mild, probable generalized anxiety that will require clinical judgement from a physician for intervention [9] [10] . The patient’s cognitive baseline is assessed using the MMSE and the clock drawing test with scores of 20/30 and 2/5 respectively. Both tests support her diagnosis of mild EOAD [11] [12] .
The difficulty with balance is indicated by a TUG score of 13 seconds which suggest an increased risk of falls [13] . The weakness she is experiencing in her L/E and difficulty with postural control and dual gait tasks are demonstrated within the Mini-BESTest reflecting a score of 21/23 [14] . Tasks of poor performance that indicate physiotherapy intervention include: reactive postural control during compensatory stepping when making corrections to forward, backward, and lateral external perturbations. There were also marked difficulties in dynamic gait when asked to speed up, turn head when walking, execute a pivot turn, and when stepping over obstacles. Fine motor skills as assessed through the finger-to-nose test, and finger opposition indicate mild dysmetria.
Problem List [ edit | edit source ]
- Decreased postural control: due to weakness with external perturbations
- Decreased balance: instability during gait, especially during dual tasks
- Decreased L/E muscle strength and proprioception
- Reduced aerobic capacity
- Decreased fine motor control and coordination
- Memory impairment: difficulty remembering instructions and task components
- Increased fatigue secondary to depression
Intervention [ edit | edit source ]
Patient goals [ edit | edit source ].
- Improve reactive postural control to external perturbations in the Mini-BESTest taking no more than 2 steps to recover balance within 2 months
- Improve TUG score from 13sec to 10sec within 8 weeks to surpass the cutoff for independent mobility
- Increase lower extremity strength on IBT by 1 point within 2 months
- Improve the accuracy of movements on the finger to nose coordination test
- Be able to walk and count by 2’s without hesitation and stopping within 8 weeks to improve motor coordination and cognition
Treatment Plan [ edit | edit source ]
Medical and lifestyle management are areas of practice addressed within the interprofessional care team. Pharmacological agents will manage cognitive function and behavioural symptoms [16] . In addition, consuming a healthy diet, such as the Mediterranean Diet (MeDi) diet may help slow cognitive decline in individuals with Alzheimer’s disease [17] .
Outcome [ edit | edit source ]
Following Mrs. S’s initial assessment it was determined she would receive four months of physiotherapy care to address her postural and gait impairments with associated fatigue. Her treatment program consisted of visits two times per week for the first month and one visit every 3 weeks for the last three months. A thorough follow-up assessment was performed.
Within four months her AROM and muscular strength improved slightly and there were no significant changes in vital signs. Mrs. S still presents with forward (protracted) head posture along with a slight postural kyphosis. She had slight improvement in her postural awareness and increased motor control of her scapulothoracic stabilizing muscles.
The scores on her outcome measures are listed below:
- FAQ = 13/30
- GAD-7 = 7/21
- PHQ-9 = 8/27
- MMSE = 20/30
- Clock drawing test = 2/5
- TUG = 10 seconds
- Mini-Best = 24/28
The GAD-7 and PHQ-9 decreased indicating a lower number of symptoms associated with anxiety and depression. This may reflect her increase in confidence with daily tasks, postural control, strength and decreased fatigue. Mrs. S improved on the gait components of the Mini-Best test, increasing her score by a total of three points. Furthermore, her TUG time on reassessment was 10 seconds which decreases her risk of falls. For the MMSE and clock drawing test no significant changes were reported. These tests will continue to be used to monitor the cognitive status over time.
Based on her progress and improvements over the past four months Mrs. S should continue physiotherapy treatment as needed to help manage the progression of the musculoskeletal, postural, and gait impairments secondary to EOAD. It is suggested she visit her family doctor to receive a referral to community balance and healthy aging programs. Mrs. S would benefit from a referral to an occupational therapist for a thorough home assessment, maintenance of mental health status and future need for assistive devices. Ms. S would further benefit from a nutritionist or dietitian who can educate her on proper eating habits such as the MeDi diet which has been shown benefit patients with Alzheimer's [17] .
Discussion [ edit | edit source ]
Mrs. S presented with a history of falls, gait deficits, and decreased cognition. Mrs. S and her physiotherapist developed a list of goals to assist with managing and preventing further progression of her mobility difficulties. After four months of the physiotherapy treatment plan, a thorough follow-up assessments was completed. Improvements where seen in her confidence to perform ADLs and a decrease in stress and anxiety. Furthermore, her L/E strength increased as well as her mobility. Other cognitive symptoms did not change which may be due to the progression of the disease.
There are many cases of EOAD presenting with gait impairments, postural instability, decreased musculoskeletal and memory function found secondary to the disease. The role of a physiotherapist varies depending on the disease progression, but the overall aim is to maximize independence by improving and preserving motor and cognitive function [2] . Although there are similarities in symptoms among patients with EOAD, the treatment plan should be personalized to each individual. However, as the disease progresses, there should be additional emphasis placed on decreasing risk of falls, managing cognitive decline and reducing the burden on family and caregivers [2] [4] .
As discussed, intervention approaches such as exercise and physical activity are beneficial for those with EOAD. These interventions are also applicable for patients with dementia and aging related cognitive impairments. The research has shown that a combination of both aerobic and strength exercise can improve physical function [4] . Participation in community and home exercise programs consisting of daily exercises and a graded walking program have shown to improve independence with performing ADLs and overall quality of life (QOL) [18] . Through improving functional ability of the patient, research suggests that home exercise programs also provide benefit to their caregivers by reducing physical and emotional burden [18] .
Rehabilitation therapy is constantly evolving and so are the needs of each individual with Alzheimer’s Disease. The progression of the disease varies in severity and time for each individual as should their treatment. Further research should be focused on bridging the gap in literature around disease progression and physiotherapy intervention focusing on determining the appropriate frequency, intensity, and duration of treatment for this population [3] [4] . The evolution of the research should focus on selecting a study design and methodical approach that will increase the external validity and thus allow for the transfer of knowledge to the EOAD cohort.
References [ edit | edit source ]
- ↑ 1.0 1.1 Alzheimer's Disease and Dementia. (2019). What Is Alzheimer's? . [online] Available at: https://www.alz.org/alzheimers-dementia/what-is-alzheimers [Accessed 9 May 2019].
- ↑ 2.0 2.1 2.2 Lord S, Rochester LY. Role of the physiotherapist in the management of dementia . 2017 Feb 24 (pp. 240-248). CRC Press.
- ↑ 3.0 3.1 3.2 Groot C, Hooghiemstra AM, Raijmakers PG, Van Berckel BN, Scheltens P, Scherder EJ, Van der Flier WM, Ossenkoppele R. The effect of physical activity on cognitive function in patients with dementia: a meta-analysis of randomized control trials . Ageing research reviews. 2016 Jan 1;25:13-23.
- ↑ 4.0 4.1 4.2 4.3 4.4 Rao AK, Chou A, Bursley B, Smulofsky J, Jezequel J. Systematic review of the effects of exercise on activities of daily living in people with Alzheimer’s disease. American Journal of Occupational Therapy . 2014 Jan 1;68(1):50-6.
- ↑ 5.0 5.1 Forbes D, Forbes SC, Blake CM, Thiessen EJ, Forbes S. Exercise programs for people with dementia . Cochrane Database of Systematic Reviews. 2015(4).
- ↑ McDonnell MN, Smith AE, Mackintosh SF. Aerobic exercise to improve cognitive function in adults with neurological disorders: a systematic review. Archives of physical medicine and rehabilitation. 2011 Jul 1;92(7):1044-52.
- ↑ Lamb SE, Sheehan B, Atherton N, Nichols V, Collins H, Mistry D, Dosanjh S, Slowther AM, Khan I, Petrou S, Lall R. Dementia And Physical Activity (DAPA) trial of moderate to high intensity exercise training for people with dementia: randomised controlled trial. bmj. 2018 May 16;361:k1675.
- ↑ Teng E, Becker BW, Woo E, Knopman DS, Cummings JL, Lu PH. Utility of the Functional Activities Questionnaire for distinguishing mild cognitive impairment from very mild Alzheimer’s disease. Alzheimer disease and associated disorders. 2010 Oct;24(4):348.
- ↑ Spitzer RL, Kroenke K, Williams JB, Löwe B. A brief measure for assessing generalized anxiety disorder: the GAD-7 . Archives of internal medicine. 2006 May 22;166(10):1092-7.
- ↑ Kroenke K, Spitzer RL, Williams JB, Löwe B. The patient health questionnaire somatic, anxiety, and depressive symptom scales: a systematic review. General hospital psychiatry. 2010 Jul 1;32(4):345-59.
- ↑ Pangman VC, Sloan J, Guse L. An examination of psychometric properties of the mini-mental state examination and the standardized mini-mental state examination: implications for clinical practice. Applied Nursing Research. 2000 Nov 1;13(4):209-13.
- ↑ Mendes-Santos LC, Mograbi D, Spenciere B, Charchat-Fichman H. Specific algorithm method of scoring the Clock Drawing Test applied in cognitively normal elderly. Dementia & neuropsychologia. 2015 Jun;9(2):128-35.
- ↑ Podsiadlo D, Richardson S. The timed “Up & Go”: a test of basic functional mobility for frail elderly persons. Journal of the American geriatrics Society. 1991 Feb;39(2):142-8.
- ↑ Leddy AL, Crowner BE, Earhart GM. Utility of the Mini-BESTest, BESTest, and BESTest sections for balance assessments in individuals with Parkinson disease. Journal of neurologic physical therapy: JNPT. 2011 Jun;35(2):90.
- ↑ Jensen LE, Padilla R. Effectiveness of interventions to prevent falls in people with Alzheimer’s disease and related dementias. American Journal of Occupational Therapy. 2011 Sep 1;65(5):532-40.
- ↑ Bishara D, Sauer J, Taylor D. The pharmacological management of Alzheimer's disease. Progress in Neurology and Psychiatry. 2015 Jul;19(4):9-16.
- ↑ 17.0 17.1 Frisardi V, Panza F, Seripa D, Imbimbo BP, Vendemiale G, Pilotto A, Solfrizzi V. Nutraceutical properties of Mediterranean diet and cognitive decline: possible underlying mechanisms. Journal of Alzheimer's Disease. 2010 Jan 1;22(3):715-40.
- ↑ 18.0 18.1 Vreugdenhil A, Cannell J, Davies A, Razay G. A community‐based exercise programme to improve functional ability in people with Alzheimer’s disease: A randomized controlled trial . Scandinavian journal of caring sciences. 2012 Mar;26(1):12-9.
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Alzheimer’s Disease, Case Study Example
Pages: 6
Words: 1533
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Introduction
Alzheimer’s Disease is a complex and challenging health concern which impacts millions of older adults throughout the world. The pathophysiologic nature of this condition is difficult to treat and prevent further decline. Many patients suffer significant brain dysfunction and memory loss resulting from Alzheimer’s Disease; therefore, it is necessary to evaluate this condition from the perspective of a specific case study and the potential pathophysiologic causes of the disease. It is expected that the case study description will address further considerations that impact the patient’s condition and how to optimize treatment methods to manage the disease at a successful level. The following discussion will evaluate a specific case study and will recognize the importance of pathophysiology in the diagnosis and treatment of Alzheimer’s Disease for this patient population.
Alzheimer’s Disease is a condition that impacts the brain and leads to a gradual decline in cognitive function, including the loss of memory and the ability to perform routine activities (“Chapter 20”). Common symptoms include aphasia, visual disturbances, the ability to reason and concentrate, and other related factors (“Chapter 20”). Approximately 4.5 million cases of the disease currently exist in the United States and continue to challenge researchers and clinicians in their efforts to discover and utilize treatments for this condition. Case studies provide specific information regarding patients with this condition and the different treatments that are available to manage its symptoms more effectively in the context of alleviating symptoms through different methods.
The patient is a 76 year-old female who has recently become socially withdrawn and less than enthusiastic regarding her prior activities (Kongable, 2006). Recent events demonstrate her lack of clarity and significant confusion regarding different public events, in spite of having no recent bouts of illness or infection (Kongable, 2006). The patient was brought into the emergency department for an examination and was anxious upon arrival with normal vital signs and no signs of physical abnormalities (Kongable, 2006). Upon review of her laboratory results, normal values were identified; however, her MMSE demonstrated three types of cognitive deficits and memory impairment (Kongable, 2006). Furthermore, the Geriatric Depression Scale favored memory challenges, poor sleeping habits, an apathetic tone, and increased dependence on others (Kongable, 2006). These latter factors are typical signs of Alzheimer’s Disease for this population group (Kongable, 2006).
The pathophysiology of Alzheimer’s Disease is complex and may be attributed to four specific gene mutations, in addition to different types of tissue mutations that contribute to this condition, such as a reduced levels of choline acetyltransferase and cell death for some neurons (“Chapter 20”). In addition, there tends to be an expanded level of production of B-Amyloid in neuronal cells and interferes with learning and memory signaling (“Chapter 20”). These contributions to the disease become progressively worse over time and lead to severe cognitive deficits and other incapacities for many patients with this condition (“Chapter 20”). The interferlence of routine neuronal growth and function is likely to create deficits in cognition that are irreversible and difficult to treat in many ways (“Chapter 20”).
Alzheimer’s Disease is historically complex and difficult to treat. In addition, testing for this disease is not universal for all patients; rather, it is the responsibility of the clinician to determine this diagnosis by examining symptoms and evaluating existing profiles for the disease (Mayo Clinic, 2013). Furthermore, neuropsychological testing is necessary for some patients to determine the type and level of dementia that a patient is currently experiencing (Mayo Clinic, 2013). Finally, brain imaging is required in some cases, including CT Scans and MRI testing to form a definitive diagnosis (Mayo Clinic, 2013). In the case study, the patient has a number of classic Alzheimer’s symptoms; therefore, the diagnosis is Alzheimer’s Disease.
For this patient and for many other patients, the effective treatment of Alzheimer’s Disease is very difficult and challenging for a number of reasons. It is important for patients to be evaluated and diagnosed as early as possible so that they are provided with the best possible options for treatment (Salloway and Correia, 2009). Currently, there are five pharmacologic alternatives available to treat patients with Alzheimer’s Disease, including a group of cholinesterase inhibitors such as Tacrine, Donepezil and Galantime, along with Memantine (Salloway and Correia, 2009). It is known that “The main benefit of the cholinesterase inhibitors in clinical trials is an attenuation of decline over time rather than an improvement in cognitive or behavioral symptoms. This should be considered when judging whether there has been a positive effect” (Salloway and Correia, 2009). Therefore, it is necessary to determine how to best approach the treatment of Alzheimer’s Disease for patients not with the intent to cure the disease, but to delay or reduce the impact of its various symptoms for as long as possible (Salloway and Correia, 2009).
For each patient who is diagnosed with Alzheimer’s Disease, it is important to evaluate the strength of different treatment methods and how they might support improved symptom management over time. For the case study patient, a cholinesterase inhibitor is likely to lead to the improvement of symptoms, but also depends on the stage of the condition at the time of diagnosis (Shah et.al, 2008). For current patients with the disease, the limited number of pharmacologic treatments that are available is likely to be troublesome; however, the progression of the disease and its specific causes lead to complex underlying issues that are difficult to manage, particularly when changes to the genetic makeup of neurons are evident (Shah et.al, 2008). Establishing an effective treatment plan for a given patient is challenging because the outcomes at best are the delayed onset of symptoms in some cases (Shah et.al, 2008).
Future directions for Alzheimer’s Disease represent a challenge to researcher and clinicians alike due to the complexities of this condition. It is known that “AD and other neurodegenerative disorders are associated with oxidative and inflammatory stress and mitochondrial dysfunction… In the neurobiology underlying the development of AD, there is a progression of hyperphosphorylated tau-bearing tangles appearing initially in the entorhinal cortex and hippocampus, then progressing to neocortex of the temporal, frontal, and parietal cortices. An optimal disease-modifying strategy should interfere with this cascade either by interfering with an upstream causal event (thought by many to be generation of Aβ) or targeting tangle formation directly” (Rafii and Aisen, 2009). Under these circumstances, it is necessary to continue research in order to develop new treatment methods for Alzheimer’s patients at different stages of the disease (Rafii and Aisen, 2009).
Patients with Alzheimer’s Disease are very challenging to clinicians and researchers alike because the ability to manage the disease has been realized for some patients, while others faced advanced cognitive impairment that cannot be alleviated or reversed (“Chapter 20”). Under these conditions, it is expected that disease progression will move forward on a gradual basis and will impact each patient in different ways. Nonetheless, the continued development of B-amyloid therapeutics is the primary objective of many scientists as a means of reducing the time progression of the disease (Rafii and Aisen, 2009). It is important for scientists to examine specific tissue forms and neurons to determine functionality and any mutations that exist in order to develop treatments that will slow these actions as best as possible to achieve optimal treatment outcomes for these patients (Rafii and Aisen, 2009).
Understanding Alzheimer’s Disease as a complex condition with many variables is perhaps the most effective means of recognizing the severity and devastation of the disease. Its pathophysiology has been determined to be the cause of genetic mutations and neuronal cell changes that contribute to eventual cell death and cognitive decline (“Chapter 20”). Therefore, it is important to evaluate each case individually and to determine the extent of the symptoms and the stage of the disease (“Chapter 20”). It is important to evaluate these considerations and the steps that are necessary to provide effective treatment to patients according to their specific symptoms and level of cognition.
For the patient in the example case study, due to the patient’s level of cognition and memory loss, she should be prescribed a cholinesterase inhibitor such as Tacine or Donepezil to treat the condition and to reduce the production of B-amyloid as best as possible. If this treatment method is successful, it will reduce the severity of current symptoms and prolong the condition for a longer period of time so that the patient’s quality of life is not minimized in a significant manner. From a non-pharmacologic perspective, it is also important to provide the patient with the means to preserve her quality of life as best as possible by attempting to provide a sense of normalcy and encouragement, in spite of her memory and cognitive deficits. This is perhaps the most relevant means of promoting a greater quality of life for the patient with the current state of her condition.
“Chapter 20: Alzheimer Disease.” 283-290.
Kongable, G. (2006). Case Study: Alzheimer Disease.
Raafi, M.S., and Aisen, P.S. (2009). Recent developments in Alzheimer’s Disease therapeutics. BMC Medicine, 7(7), 1-4.
Salloway, S., and Correia, S. (2009). Alzheimer disease: time to improve its diagnosis and treatment. Cleveland Clinic Journal of Medicine, 76(1), 49-58.
Shah, R.S., Lee. H.G., Zhu, X., Perry, G., Smith, M.A., and Castellani, R.J. (2008). Current approaches in the treatment of Alzheimer’s Disease. Biomedicine & Pharmacotherapy, 62(4), 199-207.
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Alzheimer’s Disease Case Study
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- Models of Care Case Studies
The Alzheimer’s Association is committed to connecting clinicians to effective, evidence-based models of care that can be replicated in community settings. Two of these models — the UCLA Alzheimer’s and Dementia Care program and the Age-Friendly Health Systems initiative — are detailed below.
UCLA Alzheimer's and Dementia Care program Age-Friendly Health Systems initiative UCLA Alzheimer’s and Dementia Care program
A dementia-specific model of care that significantly improved the experience for caregivers and people living with the disease.
About the program
The Alzheimer’s Association has partnered with UCLA to replicate the UCLA Alzheimer’s and Dementia Care (ADC) program through a grant from the John A. Hartford Foundation. The program follows a co-management model within the UCLA health system and partners with community-based organizations (CBOs) to provide comprehensive, coordinated, individualized care for people living with Alzheimer’s disease and other dementias.
The goals of the program are to:
- Maximize function, independence and dignity for people living with dementia.
- Minimize caregiver strain and burnout.
- Reduce unnecessary costs through improved care.
To qualify for the program, participants must have a diagnosis of dementia and live outside of a nursing home. The mean age of the first program participants was 82 years old. Almost all of the caregivers were the children (59%) or spouses (41%) of individuals living with Alzheimer’s or other dementias.
Comprehensive care
The ADC program utilizes a co-management model in which a nurse practitioner Dementia Care Specialist (DCS) partners with the participant’s primary care doctor to develop and implement a personalized care plan. The DCS provides support via four key components:
- Conducting in-person needs assessments of individuals living with Alzheimer’s and their caregivers.
- Creating and implementing individualized dementia care plans.
- Monitoring and revising care plans, as needed.
- Providing access 24/7, 365 days a year for assistance and advice to help avoid Emergency Department (ED) visits and hospitalizations.
Community resources
The ADC program also connects caregivers with resources provided by CBOs, including:
- Adult day care.
- Counseling.
- Case management.
- Legal and financial advice.
- Workforce development focused on training families and caregivers.
Program effectiveness
At one year, the quality of care provided by the program as measured by nationally accepted quality measures for dementia was exceedingly high — 92% compared to a benchmark of 38%. As a result, the improvements experienced by both caregivers and patients were significant:
- Ninety-four percent of caregivers felt that their role was supported.
- Ninety-two percent would recommend the program to others.
- Confidence in handling problems and complications of Alzheimer’s and other dementias improved by 79%.
- Caregiver distress related to behavioral symptoms, depression scores and strain improved by 31%, 24% and 15%, respectively.
- Despite disease progression, behavioral symptoms like agitation, irritability, apathy and nighttime behaviors in people living with dementia improved by 22%.
- Depressive symptoms experienced by individuals living with the disease were reduced by 34%.
Cost benefits of the program
An external evaluator compared utilization and cost outcomes and determined that over the course of 3 1/2 years, participants in UCLA’s program had lower total Medicare costs of care ($2,404 per year) relative to those receiving usual care.
In addition to cost savings for individuals and their families, the ADC program reports several financial benefits for health systems, including:
- Hospitalizations: 12% reduction
- ED visits: 20% reduction
- ICU stays: 21% reduction
- Hospital days: 26% reduction
- Hospice in last six months: 60% increase
- Nursing home placement: 40% reduction
UCLA finds that a care program following the ADC model may be able to pay for itself depending on local labor costs, comprehensiveness of billing and local overhead applied to clinical revenue.
To learn more or to contact UCLA about training and replication of the program, visit the UCLA Alzheimer’s and Dementia Care Program website.
Age-Friendly Health Systems initiative
A model of care that incorporates person-centered dementia care into a broader framework for the care of older adults.
About the initiative
Age-Friendly Health Systems is an initiative of The John A. Hartford Foundation and the Institute for Healthcare Improvement (IHI) in partnership with the American Hospital Association (AHA) and the Catholic Health Association of the United States (CHA). Together in 2017, they set a bold vision to build a social movement so all care with older adults is age-friendly care, that:
- Follows an essential set of evidence-based practices.
- Causes no harm.
- Aligns with “What Matters” to the older adult and their family caregivers.
The Age-Friendly Health Systems initiative defines “What Matters” as knowing and aligning care with each older adult’s specific health outcome goals and care preferences including, but not limited to, end-of-life care, and across settings of care.
- Health outcome goals relate to the values and activities that matter most to an individual, help motivate the individual to sustain and improve health, and could be impacted by a decline in health — for example, babysitting a grandchild, walking with friends in the morning, or volunteering in the community. When identified in a specific, actionable, and reliable manner, patients’ health outcome goals can guide decision making.
- Care preferences include the health care activities (e.g., medications, self-management tasks, health care visits, testing, and procedures) that patients are willing and able (or not willing or able) to do or receive.
The 4Ms framework of an Age-Friendly Health System
The 4Ms are not a program, but a framework to guide how care is provided to older adults through every interaction with a health system’s care and services. The 4Ms — What Matters, Medication, Mentation, and Mobility — make the complex care of older adults more manageable because they:
- Identify the core issues that should drive all care and decision making with the care of older adults.
- Organize care and focus on the older adult’s wellness and strengths rather than solely on disease.
- Are relevant regardless of an older adult’s individual disease(s).
- Apply regardless of the number of functional problems an older adult may have, or that person’s cultural, ethnic or religious background.
The 4Ms framework is most effective when all 4Ms are implemented together and are practiced reliably (i.e., for all older adults, in all settings and across settings, in every interaction).
The intention is to incorporate the 4Ms into existing care — rather than layering them on top —to organize the efficient delivery of effective care. This is achieved primarily through redeploying existing health system resources. Many health systems have found they already provide care aligned with one or more of the 4Ms for many of their older adult patients. Much of the effort, then, is to incorporate the other elements and organize care so all 4Ms guide every encounter with an older adult and their family caregivers.
Cost benefits of the initiative
The business case for becoming an Age-Friendly Health System focuses on its financial returns and is stronger when:
- The financial benefits are captured by the health system that is making the investment.
- Utilization and associated expenses of “usual” care are especially burdensome.
- The health system is effective in mitigating those costs.
- The added expense of becoming age-friendly is lower.
See the IHI report, The Business Case for Becoming an Age-Friendly Health System , for guidance on how to make the business case for your health system.
To learn more or to contact IHI about joining the initiative, visit the IHI Age-Friendly Health Systems website.
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Case Study on Alzheimer’s Disease
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CASE STUDY ON ALZHEIMER’S DISEASE
Running head: CASE STUDY ON ALZHEIMER’S DISEASE
May 1, 2019
Introduction
This case study involves a 76-year-old Iranian male, Mr. Akkad, who suffers from a major neurocognitive disorder presumably caused by Alzheimer’s disease. He presents with severe disorientation to time and events and partial orientation to place. He has impaired insight and judgement and tends to stray away his line of thought in a conversation. Also, Mr. Akkad exhibits limitations in his registration, attention, calculation, and memory. In fact, there are noticeable confabulations in various aspects of his memory. His affect is restricted which means that his display of emotions and feelings towards other people is limited. In summation, Mr. Akkad presents a decline in cognitive ability due to a neurodegenerative illness known as Alzheimer’s disease.
In this case study, Mr. Akkad lives with his family and the primary caregiver seems to be his eldest son who brings him to the hospital. The care setting of the client is of vital importance to his manageability of the illness. During the consultation the PMHNP conducts a Mini-Mental State Exam which reveals that Mr. Akkad may have moderate dementia. Further diagnosis shows that he has Alzheimer’s disease which is a type of dementia. He is often forgetful and loses orientation to place, time and events. This aspect is crucial in developing a treatment plan for Mr. Akkad. Nonetheless, the client is generally co-operative during his consultation and appears to enjoy conversation.
Purpose of essay
The aim is to develop an individualized drug regimen for the client’s neurocognitive disorder.
There were three options of drugs listed for treatment. The first choice was administering rivastigmine 1.5mg orally twice a day and the dosage would increase to 3mg in two weeks. The second option was Aricept (donepezil) at a dose of 5mg to be taken orally at bedtime. The last choice was Razadyne (galantamine) administered at 4mg orally twice a day. The suitable option at this point was Aricept (donepezil) which would be taken at a dosage of 5mg orally. This drug is appropriate because it is a cholinesterase inhibitor approved by the Food and Drug Administration to treat all stages of Alzheimer’s disease. Alzheimer’s Association (2017) writes that Aricept is best known for treatment all stages of Alzheimer’s but mostly prescribed for moderate to severe Alzheimer’s. In this case scenario, Mr. Akkad presents with major neurocognitive disorders which means shows the severity of his condition. Therefore, Aricept would be the best fit. The first choice of rivastigmine was unsuitable as it is mostly prescribed for mild to moderate Alzheimer’s. Furthermore, Foster et al. (2016) conducted a study to investigate which drug between Rivastigmine and donepezil was more effective in treating Alzheimer’s disease. The findings revealed that donepezil was more effective because of the region of the brain that it targets. Donepezil caused increase blood flow to the anterior frontal lobe and parietal lobe while rivastigmine increased the flow to the hippocampal region and prefrontal cortex. The areas targeted by the donepezil drug are associated with vigilant attention and working memory. Hence, patients who use it performed better compared to those who use rivastigmine. The last option, Razadyne, was also a poor option because it is often used to treat mild to moderate Alzheimer’s and would be inefficient in treating Mr. Akkad’s severe Alzheimer’s. The goal of this treatment was to reduce the patient’s cognitive decline. The outcome of the donezepil drug was not as expected. It did not improve the patient’s condition at all. The difference may have been caused by the dosage of 5mg daily. Seemingly, a higher dose may bring the expected results. Also, a different drug may also be necessary.
The options available at this point were to increase the Aricept drug to a dosage of 10mg per day to be taken orally. The second choice was to discontinue Aricept and begin galantamine drug extended release at a dose of 24mg orally daily. The last option was to discontinue Aricept and administer memantine extended release at 28mg orally daily. The best option is to increase the dosage of Aricept to 10mg orally to be taken at bedtime. This choice is suitable because it would give a chance for confirmation that donepezil is effective or completely ineffective on the patient. Cummings et al. (2015) report that during a clinical trial, an increased dose of donezepil, from 10mg and above, for moderate to severe Alzheimer’s portrayed an increased cognitive ability on the patients. The second and third option of discontinuing donezepil and starting galantamine extended release or memantine extended release was unfavorable because risk of withdrawal symptoms. Bond et al. (2012) explain that withdrawal of donezepil will often be accompanied by worsening of symptoms. The article adds that initial lack of benefits from the donezepil drug is common but the drug will later respond. The goal of this treatment was to improve the efficacy of donezepil thus improving the cognitive ability of the patient. The outcome was not as expected. The patient showed slight improvement but most of the cognitive issues were still prominent. The difference between the expectation and the outcome is that the drug donezepil is not appropriate for Mr. Akkad. Yan & Chen (2016) state that drug treatment of Alzheimer’s disease is often effective for only half of the patients. Therefore, it is probable that Mr. Akkad needed a different drug for treatment.
The options present were to continue with Aricept at the same 10mg dosage. The second choice was to increase the dosage of Aricept to 15mg for six weeks after which the dose will be increased to 20mg. The third alternative was to discontinue Aricept and begin Namenda drug at 5mg daily orally. The most suitable course of action was to discontinue Aricept and begin administering the new drug, Namenda at 5mg daily. This choice was appropriate because the Aricept drug proved to be ineffective in alleviating the patient’s condition. Increasing the dosage of the Aricept drug only showed very little effectiveness. The first choice was not appropriate because sticking to the same drug would most likely have no benefits to the patient. The second option was to increase the dosage which was also not a good alternative since the improvement shown will likely be very slight. The goal of the treatment is to improve the cognitive ability of the patient. According to the outcome, the patient showed improvement in his willingness to attend religious activities. However, his disinhibition was not guaranteed to change. This result was not as expected. Discontinuing Aricept was not a good choice due to withdrawal effect. Instead, adding Namenda as combined therapy was the best route.
The best drug regimen for Mr. Akkad was the combined therapy of Aricept and Namenda. In terms of ethical consideration, properly informing the patient and caregivers is crucial to the treatment plan. In this case, the eldest son was well involved which helped with the follow-up consultations. Aside from this, all the drugs administered were FDA approved.
Alzheimer’s Association. (2017). FDA-approved treatments for Alzheimer’s. Retrieved from https://www.alz.org/media/Documents/fda-approved-treatments-alzheimers-ts.pdf
Bond, M., Rogers, G., Peters, J., Anderson, R., Hoyle, M., Miners, A., Moxham, T., & Davis, S. (2012). The effectiveness and cost-effectiveness of donepezil, galantamine, rivastigmine and memantine for the treatment of Alzheimer’s disease (Review of Technology Appraisal No. 111): a systematic review and economic model. Health Technology Assessment, 16(1), 470-490.
Cummings, J., Isaacson, R., Schmitt, F., & Velting, D. (2015). A practical algorithm for managing Alzheimer’s disease: what, when, and why? Annals of Clinical and Translational Neurology, 2(3), 307-323.
Foster, S., Drago, V., Roosa, M., Campbell, W., Witt, C., & Heilman, K. (2016). Donepezil Versus Rivastigmine in Patients with Alzheimer’s disease: Attention and Working Memory. Journal of Alzheimer’s and Neurodegenerative Diseases, 22(2), 1-5.
Yang, K., & Chen, H. (2016). Probabilistic Cost-Effectiveness Analysis of Vaccination for Mild or Moderate Alzheimer’s Disease. Current Alzheimer’s Research, 13(7), 809-816.
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A case-control study of Alzheimer's disease
Affiliation.
- 1 Battelle Seattle Research Centers, WA 98105-5428.
- PMID: 2285263
- DOI: 10.1002/ana.410280607
A case-control study of Alzheimer's disease (AD) was conducted to evaluate the roles of family history of dementing disease and AD, and medical conditions, particularly those related to the viral and immune hypotheses in AD. One hundred and eighty-three clinically diagnosed patients were identified between 1980 and 1985 through the Geriatric and Family Services clinic at the University of Washington hospital, and 18 patients were identified during the same time period through the Veteran's Administration Medical Center in Seattle, Washington. Telephone interviews were conducted with spouses (87.7%) and children (12.3%) of the patients. Each patient was matched to a friend or nonblood relative of the patient by age, sex, and the relationship between the patient and his or her respondent, for a total of 130 matched pairs. The odds ratio for AD was elevated if a first-degree relative was reported to have a history of dementia (odds ratio, 2.21; 95% confidence interval, 1.17 to 4.18). This risk was especially elevated if a sibling was affected (odds ratio, 4.04; 95% confidence interval, 1.37 to 11.90); the highest risk to the proband was observed if a sibling had presumed AD (odds ratio, 5.92; 95% confidence interval, 1.59 to 21.96). The risk increased with increasing numbers of first-degree family members affected for both a history of dementia and presumed AD. We found little difference between patients and control subjects with respect to the age of the mother or father at the time of the subject's birth. No statistically significant differences were observed between the two groups with regard to conditions that might support the immune and viral hypothesis in AD, smoking, or alcohol problems.
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Alzheimer's disease is a brain disorder that gets worse over time. It's characterized by changes in the brain that lead to deposits of certain proteins. Alzheimer's disease causes the brain to shrink and brain cells to eventually die. Alzheimer's disease is the most common cause of dementia — a gradual decline in memory, thinking, behavior and social skills. These changes affect a person's ability to function.
About 6.5 million people in the United States age 65 and older live with Alzheimer's disease. Among them, more than 70% are 75 years old and older. Of the about 55 million people worldwide with dementia, 60% to 70% are estimated to have Alzheimer's disease.
The early signs of the disease include forgetting recent events or conversations. Over time, it progresses to serious memory problems and loss of the ability to perform everyday tasks.
Medicines may improve or slow the progression of symptoms. Programs and services can help support people with the disease and their caregivers.
There is no treatment that cures Alzheimer's disease. In advanced stages, severe loss of brain function can cause dehydration, malnutrition or infection. These complications can result in death.
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Memory loss is the key symptom of Alzheimer's disease. Early signs include difficulty remembering recent events or conversations. But memory gets worse and other symptoms develop as the disease progresses.
At first, someone with the disease may be aware of having trouble remembering things and thinking clearly. As symptoms get worse, a family member or friend may be more likely to notice the issues.
Brain changes associated with Alzheimer's disease lead to growing trouble with:
Everyone has memory lapses at times, but the memory loss associated with Alzheimer's disease persists and gets worse. Over time, memory loss affects the ability to function at work or at home.
People with Alzheimer's disease may:
- Repeat statements and questions over and over.
- Forget conversations, appointments or events.
- Misplace items, often putting them in places that don't make sense.
- Get lost in places they used to know well.
- Eventually forget the names of family members and everyday objects.
- Have trouble finding the right words for objects, expressing thoughts or taking part in conversations.
Thinking and reasoning
Alzheimer's disease causes difficulty concentrating and thinking, especially about abstract concepts such as numbers.
Doing more than one task at once is especially difficult. It may be challenging to manage finances, balance checkbooks and pay bills on time. Eventually, a person with Alzheimer's disease may be unable to recognize and deal with numbers.
Making judgments and decisions
Alzheimer's disease causes a decline in the ability to make sensible decisions and judgments in everyday situations. For example, a person may make poor choices in social settings or wear clothes for the wrong type of weather. It may become harder for someone to respond to everyday problems. For example, the person may not know how to handle food burning on the stove or decisions when driving.
Planning and performing familiar tasks
Routine activities that require completing steps in order become a struggle. This may include planning and cooking a meal or playing a favorite game. Eventually, people with advanced Alzheimer's disease forget how to do basic tasks such as dressing and bathing.
Changes in personality and behavior
Brain changes that occur in Alzheimer's disease can affect moods and behaviors. Problems may include the following:
- Depression.
- Loss of interest in activities.
- Social withdrawal.
- Mood swings.
- Distrust in others.
- Anger or aggression.
- Changes in sleeping habits.
- Loss of inhibitions.
- Delusions, such as believing something has been stolen.
Preserved skills
Despite major changes to memory and skills, people with Alzheimer's disease are able to hold on to some skills even as symptoms get worse. Preserved skills may include reading or listening to books, telling stories, sharing memories, singing, listening to music, dancing, drawing, or doing crafts.
These skills may be preserved longer because they're controlled by parts of the brain affected later in the course of the disease.
When to see a doctor
A number of conditions can result in memory loss or other dementia symptoms. Some of those conditions can be treated. If you are concerned about your memory or other thinking skills, talk to your health care provider.
If you are concerned about thinking skills you observe in a family member or friend, talk about your concerns and ask about going together to talk to a provider.
More Information
Alzheimer's disease care at Mayo Clinic
- Alzheimer's stages
- Memory loss: When to seek help
- Sundowning: Late-day confusion
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- Healthy brain and brain with Alzheimer's disease
In the brain of someone with Alzheimer's disease, amyloid plaques form and tau proteins change shape and become tangles.
The exact causes of Alzheimer's disease aren't fully understood. But at a basic level, brain proteins fail to function as usual. This disrupts the work of brain cells, also called neurons, and triggers a series of events. The neurons become damaged and lose connections to each other. They eventually die.
Scientists believe that for most people, Alzheimer's disease is caused by a combination of genetic, lifestyle and environmental factors that affect the brain over time. In less than 1% of cases, Alzheimer's is caused by specific genetic changes that almost guarantee a person will develop the disease. In these cases, the disease usually begins in middle age.
The development of the disease begins years before the first symptoms. The damage most often starts in the region of the brain that controls memory. The loss of neurons spreads in a somewhat predictable pattern to other regions of the brain. By the late stage of the disease, the brain has shrunk significantly.
Researchers trying to understand the cause of Alzheimer's disease are focused on the role of two proteins:
- Plaques. Beta-amyloid is a fragment of a larger protein. When these fragments clump together, they appear to have a toxic effect on neurons and to disrupt communication between brain cells. These clumps form larger deposits called amyloid plaques, which also include other cellular debris.
- Tangles. Tau proteins play a part in a brain cell's internal support and transport system to carry nutrients and other essential materials. In Alzheimer's disease, tau proteins change shape and organize into structures called neurofibrillary tangles. The tangles disrupt the transport system and cause damage to cells.
- Mayo Clinic Minute: Women and Alzheimer's Disease
Risk factors
Increasing age is the greatest known risk factor for Alzheimer's disease. Alzheimer's isn't a part of typical aging. But as you grow older, the chances of developing it increases.
One study found that every year there were four new diagnoses per 1,000 people ages 65 to 74. Among people ages 75 to 84, there were 32 new diagnoses per 1,000 people. For those 85 and older, there were 76 new diagnoses per 1,000 people.
Family history and genetics
The risk of developing Alzheimer's is somewhat higher if a first-degree relative — your parent or sibling — has the disease. Just how genes among families affect the risk is largely unexplained, and the genetic factors are likely complex.
A better understood genetic factor is a form of the apolipoprotein E (APOE) gene. A form of the gene, APOE e4, increases the risk of Alzheimer's disease. About 25% to 30% of the population carries an APOE e4 allele. But not everyone with this form of the gene develops the disease.
Scientists have found rare changes in three genes that virtually guarantee a person who inherits one of them will develop Alzheimer's. But these changes account for less than 1% of people with Alzheimer's disease.
Down syndrome
Many people with Down syndrome develop Alzheimer's disease. This is likely related to having three copies of chromosome 21. Chromosome 21 is the gene involved in the production of the protein that leads to the creation of beta-amyloid. Beta-amyloid fragments can become plaques in the brain. Symptoms tend to appear 10 to 20 years earlier in people with Down syndrome than they do for the general population.
Overall there are more women with the disease because they tend to live longer than men.
Mild cognitive impairment
Someone with mild cognitive impairment (MCI) has a decline in memory or other thinking skills that is greater than usual for the person's age. But the decline doesn't prevent the person from functioning in social or work environments.
However, people with MCI have a significant risk of developing dementia. When MCI affects mainly memory, the condition is more likely to progress to dementia due to Alzheimer's disease. A diagnosis of MCI offers people the chance to put a greater focus on healthy lifestyle changes and to come up with strategies to make up for memory loss. They also can schedule regular health care appointments to monitor symptoms.
Head trauma
Several large studies found that people age 50 years or older who had a traumatic brain injury (TBI) had an increased risk of dementia and Alzheimer's disease. The risk is even higher in people with more-severe and multiple TBIs . Some studies found that the risk may be greatest within the first six months to two years after the injury.
Air pollution
Studies in animals have found that air pollution particulates can speed the breakdown of the nervous system. And human studies have found that air pollution exposure — especially from traffic exhaust and burning wood — is linked to a greater dementia risk.
Excessive alcohol consumption
Drinking large amounts of alcohol has long been known to cause brain changes. Several large studies and reviews found that alcohol use disorders were linked to an increased risk of dementia — early-onset dementia in particular.
Poor sleep patterns
Research has shown that poor sleep patterns, such as trouble falling asleep or staying asleep, are linked to an increased risk of Alzheimer's disease.
Lifestyle and heart health
Research has shown that the same risk factors associated with heart disease also may increase the risk of dementia. It's unclear if these factors increase risk of dementia by worsening Alzheimer's changes in the brain or by leading to brain vascular changes. They include:
- Lack of exercise.
- Smoking or exposure to secondhand smoke.
- High blood pressure.
- High cholesterol.
- Poorly controlled type 2 diabetes.
These factors can all be modified. Therefore, changing lifestyle habits can to some degree alter your risk. For example, regular exercise and a healthy low-fat diet rich in fruits and vegetables are related to a lower risk of Alzheimer's disease.
Lifelong learning and social engagement
Studies have found that socializing and engaging in activities that stimulate the mind throughout life can lower the risk of Alzheimer's disease. Low education levels — less than a high school education — appear to be a risk factor for Alzheimer's disease.
Complications
Alzheimer's symptoms such as memory loss, language loss, impaired judgment and other brain changes can make it harder to manage other health conditions. A person with Alzheimer's disease may not be able to:
- Tell someone about being in pain.
- Explain symptoms of another illness.
- Follow a treatment plan.
- Explain medicine side effects.
As Alzheimer's disease moves into its last stages, brain changes begin to affect physical functions. The changes can affect the ability to swallow, balance, and control bowel and bladder movements. These effects can lead to other health problems such as:
- Inhaling food or liquid into the lungs.
- Flu, pneumonia and other infections.
- Poor nutrition or dehydration.
- Constipation or diarrhea.
- Dental problems such as mouth sores or tooth decay.
Alzheimer's disease is not a preventable condition. However, a number of lifestyle risk factors can be modified.
Evidence suggests that taking steps to reduce the risk of cardiovascular disease may also lower your risk of developing dementia.
To follow heart-healthy lifestyle choices that may reduce the risk of dementia:
- Exercise regularly.
- Eat a diet of fresh produce, healthy oils and foods low in saturated fat, such as a Mediterranean diet.
- Follow treatment guidelines to manage high blood pressure, diabetes and high cholesterol.
- If you smoke, ask your health care provider for help to quit.
One large, long-term study done in Finland found that making lifestyle changes helped reduce cognitive decline among people who were at risk of dementia. Those in the study were given individual and group sessions that focused on diet, exercise and social activities.
In another study done in Australia, people at risk of dementia were given coaching sessions on diet, exercise and other lifestyle changes. They had better results on cognitive tests after one, two and three years compared to people who didn't receive the coaching.
Other studies have shown that staying engaged mentally and socially is linked to preserved thinking skills later in life and a lower risk of Alzheimer's disease. This includes going to social events, reading, dancing, playing board games, creating art, playing an instrument and other activities.
- Alzheimer's disease: Can exercise prevent memory loss?
- Alzheimer's prevention: Does it exist?
- Jankovic J, et al., eds. Alzheimer disease and other dementias. In: Bradley and Daroff's Neurology in Clinical Practice. 8th ed. Elsevier; 2022. https://www.clinicalkey.com. Accessed Sept. 21, 2022.
- Alzheimer's disease fact sheet. National Institute on Aging. https://www.nia.nih.gov/health/alzheimers-disease-fact-sheet. Accessed Oct. 3, 2022.
- Livingston G, et al. Dementia prevention, intervention, and care: 2020 report of The Lancet Commission. The Lancet. 2020; doi:10.1016/S0140-6736(20)30367-6.
- Chen L, et al. Plasma tau proteins for the diagnosis of mild cognitive impairment and Alzheimer's disease: A systematic review and meta-analysis. Frontiers in Aging Neuroscience. 2022; doi:10.3389/fnagi.2022.942629.
- Dementia. World Health Organization. https://www.who.int/news-room/fact-sheets/detail/dementia. Accessed Oct. 3, 2022.
- Alzheimer's disease and related dementias. Centers for Disease Control and Prevention. https://www.cdc.gov/aging/aginginfo/alzheimers.htm. Accessed Oct. 3, 2022.
- What is dementia? Symptoms, types, and diagnosis. National Institute on Aging. https://www.nia.nih.gov/health/diagnosing-dementia. Accessed Oct. 3, 2022.
- Biomarkers for dementia detection and research. National Institute on Aging. https://www.nia.nih.gov/health/biomarkers-dementia-detection-and-research. Accessed Oct. 3, 2022.
- Middle-stage caregiving. Alzheimer's Association. https://www.alz.org/help-support/caregiving/stages-behaviors/middle-stage. Accessed Oct. 3, 2022.
- Kellerman RD, et al. Alzheimer's disease. In: Conn's Current Therapy 2022. Elsevier; 2022. https://www.clinicalkey.com. Accessed Sept. 21, 2022.
- Ferri FF. Alzheimer disease. In: Ferri's Clinical Advisor 2023. Elsevier; 2023. https://www.clinicalkey.com. Accessed Oct. 3, 2022.
- Early-stage caregiving. Alzheimer's Association. https://www.alz.org/help-support/caregiving/stages-behaviors/early-stage. Accessed Oct. 3, 2022.
- Alzheimer's disease at a glance. National Center for Complementary and Integrative Health. https://nccih.nih.gov/health/alzheimer/ataglance. Accessed Oct. 3, 2022.
- Budson AE, et al. Alzheimer's disease. In: Memory Loss, Alzheimer's Disease, and Dementia. 3rd ed. Elsevier; 2022. https://www.clinicalkey.com. Accessed Oct. 3, 2022.
- Coping with late-stage Alzheimer's disease. National Institute on Aging. https://www.nia.nih.gov/health/coping-late-stage-alzheimers-disease. Accessed Oct. 3, 2022.
- Levenson JL, ed. Dementia. In: The American Psychiatric Association Publishing Textbook of Psychosomatic Medicine and Consultation-Liaison Psychiatry. 3rd ed. American Psychiatric Association Publishing; 2019. https://psychiatryonline.org. Accessed Oct. 3, 2022.
- Dementia: Lifestyle and management. American Geriatrics Society. https://www.healthinaging.org/a-z-topic/dementia/lifestyle. Accessed Oct. 5, 2022.
- Is Alzheimer's genetic? Alzheimer's Association. https://www.alz.org/alzheimers-dementia/what-is-alzheimers/causes-and-risk-factors/genetics. Accessed Oct. 6, 2022.
- Ami T. Allscripts EPSi. Mayo Clinic. July 6, 2022.
- Alzheimer's disease research centers. National Institute on Aging. https://www.nia.nih.gov/health/alzheimers-disease-research-centers#minnesota. Accessed Sept. 26, 2022.
- About the Alzheimer's Consortium. Arizona Alzheimer's Consortium. https://azalz.org/about/#institutes. Accessed Sept. 26, 2022.
- Graff-Radford J (expert opinion). Mayo Clinic. Sept. 30, 2022.
- Shi M, et al. Impact of anti-amyloid-β monoclonal antibodies on the pathology and clinical profile of Alzheimer's disease: A focus on aducanumab and lecanemab. Frontiers in Aging and Neuroscience. 2022; doi:10.3389/fnagi.2022.870517.
- Cummings J, et al. Alzheimer's disease drug development pipeline: 2022. Alzheimer's and Dementia. 2022; doi:10.1002/trc2.12295.
- Abdi Beshir S, et al. Aducanumab therapy to treat Alzheimer's disease: A narrative review. International Journal of Alzheimer's Disease. 2022; doi:10.1155/2022/9343514.
- Aducanumab approved for treatment of Alzheimer's disease. Alzheimer's Association. https://www.alz.org/alzheimers-dementia/treatments/aducanumab. Accessed Sept. 28, 2022.
- 2022 Alzheimer's disease facts and figures. Alzheimer's Association. https://www.alz.org/alzheimers-dementia/facts-figures. Accessed Oct. 4, 2022.
- Rosenberg A, et al. Multidomain interventions to prevent cognitive impairment, Alzheimer's disease and dementia: From FINGER to world-wide FINGERS. The Journal of Prevention of Alzheimer's Disease. 2020; doi:10.14283/jpad.2019.41.
- Bleicher K, et al. Cohort profile update: The 45 and up study. International Journal of Epidemiology. 2022; doi:10.1093/ije/dyac104.
- Graff-Radford J (expert opinion). Mayo Clinic. Oct. 6, 2022.
- Swaddiwudhipong N, et al. Pre-diagnostic cognitive and functional impairment in multiple sporadic neurodegenerative diseases. Alzheimer's and Dementia. 2022; doi:10.1002/alz.12802.
- Van Dyck CH, et al. Lecanemab in early Alzheimer's disease. New England Journal of Medicine. 2023; doi:10.1056/NEJMoa2212948.
- Leqembi (approval letter). Biologics License Application 761269. U.S. Food and Drug Administration. https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=761269. Accessed Jan. 10, 2023.
- Leqembi (prescribing information). Eisai Inc.; https://www.leqembi.com/. Accessed Jan. 10, 2023.
- FDA grants accelerated approval for Alzheimer's disease treatment. Food and Drug Administration. https://www.fda.gov/news-events/press-announcements/fda-grants-accelerated-approval-alzheimers-disease-treatment. Accessed Jan. 10, 2023.
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Case Study Hub | Samples, Examples and Writing Tips
Case study on alzheimer’s disease, alzheimer’s disease case study:.
Alzheimer’s disease is the most widespread form of dementia which has been discovered and explained in 1906 by the German psychotherapist Alois Alzheimer. As a rule Alzheimer’s disease is discovered among the elderly people who reach their 65 year of life, but there are also cases of the early Alzheimer’s disease which occurs among the younger people. According to the statistics of the year 2006 the number of the people suffering from Alzheimer’s disease in the world is equal to more than 26 million people. Every patient has his own peculiarities of the disease, but there are common symptoms which differentiate the disease from the others. At the very beginning there are disorders with the short-term memory. Unfortunately, this symptom is often not paid attention to, because this problem touches upon many elderly people because of stress. In order to detect the disease the patient is seriously monitored, his behaviour and memory is analyzed with the help of numerous methods.
We can write a Custom Case Study on Alzheimer’s Disease for you!
With the further development of the disease there is the loss of the long-term memory. The gradual loss of the functions of the organism gradually leads to death. The problem of the detection of the disease lies in the terms of its development. Sometimes the disease requires more than ten years to ‘conquer’ the organism and sometimes the terms are much shorter. When Alzheimer’s disease is diagnosed, the patient will probably live no more than 7 years. In fact there rare cases when the patients live 14 years with the disease. Nowadays the nature and the factors of the disease are not known and it is impossible to cure it but only reduce its effect on the human organism.
The problem of Alzheimer’s disease is very important and troublesome for the developed countries, because the patients with the disease are the serious burdens on the economics of the countries. Alzheimer’s disease case study is the investigation of the certain case with has occurred with the patient suffering from the disease. The student should write a complete description of the life of the patient, define his age, the symptoms of the disease, define the period of time Alzheimer’s disease has been lasting and predict the possible result of the disease and describe the methods which are applied to reduce the effect of the disease on the patient.
The difficulty of case study writing lies in the disability of students to construct the right structure and analyse the limited topic from all sides. In fact, with the assistance of a free sample case study on Alzheimer’s disease written in the Internet the student will learn about the topic more. In addition one will catch the appropriate style of writing and the analysis of the problem reading a free example case study on someone with Alzheimer’s disease.
At EssayLib.com writing service you can get a custom case study on Alzheimer’s Disease topics. Your case study will be written from scratch. We hire top-rated Ph.D. and Master’s writers only to provide students with professional case study help at affordable rates. Each customer will get a non-plagiarized paper with timely delivery. Just visit our website and fill in the order form with all paper details:
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- Review Article
- Open Access
- Published: 15 March 2023
Frequency of coexistent eye diseases and cognitive impairment or dementia: a systematic review and meta-analysis
- Ying Xu ORCID: orcid.org/0000-0002-3793-7716 1 , 2 , 3 , 4 , 5 ,
- Jack Phu 6 , 7 , 8 , 9 ,
- Htein Linn Aung 1 , 4 ,
- Negin Hesam-Shariati 1 , 2 ,
- Lisa Keay 3 , 5 , 7 ,
- Phillip J. Tully 10 ,
- Andrew Booth 11 ,
- Craig S. Anderson 3 , 4 , 12 , 13 ,
- Kaarin J. Anstey ORCID: orcid.org/0000-0002-9706-9316 1 , 2 , 5 &
- Ruth Peters 1 , 2 , 3 , 4 , 5 , 14
Eye ( 2023 ) Cite this article
44 Accesses
6 Altmetric
Metrics details
- Predictive markers
- Retinal diseases
We aim to quantify the co-existence of age-related macular degeneration (AMD), glaucoma, or diabetic retinopathy (DR) and cognitive impairment or dementia.
MEDLINE, EMBASE, PsycINFO and CINAHL were searched (to June 2020). Observational studies reporting incidence or prevalence of AMD, glaucoma, or DR in people with cognitive impairment or dementia, and of cognitive impairment or dementia among people with AMD, glaucoma, or DR were included.
Fifty-six studies (57 reports) were included but marked by heterogeneities in the diagnostic criteria or definitions of the diseases, study design, and case mix. Few studies reported on the incidence. Evidence was sparse but consistent in individuals with mild cognitive impairment where 7.7% glaucoma prevalence was observed. Prevalence of AMD and DR among people with cognitive impairment ranged from 3.9% to 9.4% and from 11.4% to 70.1%, respectively. Prevalence of AMD and glaucoma among people with dementia ranged from 1.4 to 53% and from 0.2% to 25.9%, respectively. Prevalence of DR among people with dementia was 11%. Prevalence of cognitive impairment in people with AMD, glaucoma, and DR ranged from 8.4% to 52.4%, 12.3% to 90.2%, and 3.9% to 77.8%, respectively, and prevalence of dementia in people with AMD, glaucoma and DR ranged from 9.9% to 62.6%, 2.5% to 3.3% and was 12.5%, respectively.
Conclusions
Frequency of comorbid eye disease and cognitive impairment or dementia varied considerably. While more population-based estimations of the co-existence are needed, interdisciplinary collaboration might be helpful in the management of these conditions to meet healthcare needs of an ageing population.
Trial registration
PROSPERO registration: CRD42020189484.
目的: 我们旨在量化老年黄斑变性 (AMD) 、青光眼或糖尿病视网膜疾病合并认知障碍或痴呆情况。
方法: 本文检索了MEDLINE、EMBASE、PsycINFO和CINAHL (至2020年6月) 数据库。观察性研究报道了认知障碍或痴呆患者中AMD、青光眼或糖尿病视网膜病变 (DR) 的发病率或流行率, 以及AMD、青光眼或DR患者中认知障碍或痴呆的情况。
结果: 本文共纳入了56项研究 (57份报告), 这些研究在疾病的诊断标准或定义、研究设计和病例组合方面存在着异质性。很少研究报告发病率。虽然证据少, 但在轻度认知障碍者中的证据是连续的, 观察到7.7%的青光眼发病率。认知障碍者中AMD和DR的患病率分别为3.9%至9.4%和11.4%至70.1%。痴呆症患者中AMD和青光眼的患病率分别为1.4%至53%和0.2%至25.9%。痴呆症患者中DR的患病率为11%。
患有AMD、青光眼和DR的人中认知障碍的发病率分别为8.4%至52.4%、12.3%至90.2%和3.9%至77.8%, 患有AMD、青光眼和DR的人中痴呆症的发病率分别为9.9%至62.6%、2.5%至3.3%和12.5%。
结论: 眼病合并认知障碍或痴呆的频率差异性大。虽然需要更多基于人口的共病估计, 但跨学科合作可能有助于管理这些疾病以满足老龄化人口的医疗保健需求。
Introduction
Dementia affects around 50 million people, and there are nearly 10 million new cases each year worldwide [ 1 ]. Among general populations (aged ≥60 years), the prevalence of dementia has been estimated as ranging from 4.6% in Central Europe to 8.7% in North Africa and the Middle East [ 2 ], and prevalence estimates are inevitably influenced by diagnostic criteria and information source (e.g., claims or pharmacy data, or survey) [ 3 ]. Mild cognitive impairment (MCI) is a diagnosis that refers to impaired cognition [ 4 ], which is not severe enough to interfere with independent daily functioning. MCI is not a static condition with some cases progressing to dementia and some reverting to normal cognitive function [ 4 ]. Furthermore, concerns about the heterogeneity in the diagnostic and operational criteria for MCI have also been raised [ 4 ], and MCI has been applied to cognitive impairment no dementia, age-associated memory impairment, MCI, and amnestic MCI [ 4 ]. Likely due to this heterogeneity and the age of the studied participants, there has been substantial disparity in the reported prevalence of MCI, ranging from 0.5 to 42% [ 4 ].
The retina, being an extension to the brain, is particularly relevant as a potential window to explore dementia, because of the retinal-brain embryological, anatomical, and physiological connections. Thinning of the retinal nerve fibre layer and ganglion cell inner plexiform layer measured through optical coherence tomography retina scans has been reported in individuals with MCI and Alzheimer’s disease (AD) [ 5 , 6 ]. Retinal microvascular variations have been investigated as biomarkers for cerebral microvasculature changes [ 7 ], and sparser retinal microvascular networks, increased tortuosity in the retinal vessels, and reduced blood flow are associated with cognitive decline, MCI, and dementia [ 8 , 9 , 10 ].
Eye diseases that affect the retina including age-related macular degeneration (AMD), glaucoma and diabetic retinopathy (DR) are leading causes of blindness among adults [ 11 , 12 , 13 ]. Meta-analyses of 39 and 50 population-based studies, and of individual participant data from 35 studies conducted in the USA, Europe, Asia and Australia, estimated that globally 170 million (in 2014, pooled prevalence of 8.7%), 64 million (in 2013, 3.5% of population aged 40 to 80 years), and 93 million (in 2010, 34.6% of those with diabetes) people had AMD, glaucoma and DR, respectively [ 11 , 12 , 13 ].
There are commonalities between AMD, glaucoma, or DR, and cognitive impairment or dementia. Clinically, they are all chronic and progressive, with strong family history connections and increasing incidence with age [ 14 , 15 , 16 ]. Pathophysiologically, common characteristics for AMD and AD include the presence of amyloid β in the drusen of AMD patients [ 14 ]. Amyloid β has been suggested as a target for glaucoma treatment [ 17 ] and other shared characteristics between glaucoma and dementia include common gene coding OPTINEURIN [ 18 ], neuroinflammation [ 19 ], and elevated levels of tumour necrosis factor α [ 20 ]. Common risk factors for DR, brain amyloid burden, and cognitive impairment include hyperglycaemia and insulin resistance [ 21 ].
To our knowledge, there is no existing systematic review evidence on the frequency of these eye diseases in people with cognitive impairment or dementia, or the frequency of cognitive impairment or dementia in people with these eye diseases. Knowledge of these relationships can help promote timely referral and inter-disciplinary communications between healthcare professionals, e.g., optometrists, ophthalmologists, diabetologists, geriatricians and neurologists, involved in the management of such co-morbidities.
The protocol was registered in PROSPERO (CRD42020189484). Reporting of the review was followed the Meta-analysis Of Observational Studies in Epidemiology (MOOSE) guideline and Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) checklist.
Inclusion and exclusion criteria
The population of interest included studies reporting on participants (aged ≥18 years) with any types and stages of AMD, glaucoma, DR, cognitive impairment, or dementia. Studies specifically on people with comorbid AMD, glaucoma or DR and cognitive impairment or dementia in the context of other diseases were excluded, except for those on comorbid DR and cognitive impairment or dementia in people with diabetes since DR is a complication of diabetes.
Published observational studies with consecutive, random, or convenience sampling were eligible. Studies with selective sampling were excluded. Observational study designs were accepted except for case-reports, case series, and studies of fewer than 50 participants. Outcomes were incidence and prevalence of AMD, glaucoma, or DR, in people with cognitive impairment or dementia, and/or incidence and prevalence of cognitive impairment or dementia in people with AMD, glaucoma or DR.
Search strategy and screening
Four databases were searched: MEDLINE, EMBASE, PsycINFO and CINAHL (from inception to 1 June 2020, eTable 1 ). The following search terms were used as free text or controlled vocabulary as appropriate for the corresponding database: macular degeneration, geographic atrophy or dystrophy, macular oedema, vitelliform macular dystrophy, retina degeneration, drusen, glaucoma, ocular or eye hypertension, diabetic retinopathy AND Alzheimer(s), dementia, cognitive dysfunction.
No language or publication date restriction was applied. All identified titles and abstracts were screened by at least one of three reviewers, and 20% of the titles and abstracts were screened independently by two of the three reviewers. Full texts of relevant documents were obtained and independently assessed for relevance by two reviewers. All differences were resolved by discussion with the lead reviewer until the final set was agreed. Reference lists or citation trails of the included studies were checked to identify additional studies.
Statistical analyses
To estimate frequencies, within study variances were calculated as square root of ( p × (1 − p)/n), where p is the cumulative incidence or prevalence, and n is the sample size. The cumulative incidence and prevalence rates were sorted from lowest to highest rates and plotted with 95% confidence intervals (CIs). Population-based studies were listed first in forest plots, easing visual comparisons to the other studies. Statistical heterogeneity and consistency were assessed using the standard I 2 and Q statistic, with p < 0.05 indicating heterogeneity and I 2 > 75% indicating high inconsistency. Rates were synthesized using a random effect inverse variance approach for weighting. We also conducted meta-analyses to provide summary estimates of the associations between each eye disease and cognitive impairment or dementia, based on multivariable adjusted odds ratios (ORs), relative risks (RRs), or hazard ratios (HRs). All analyses were conducted using Stata 13.
Data extraction and risk of bias assessment
Data extraction was completed by two reviewers independently and compared and compiled by the lead reviewer. Risk of bias was assessed using the risk of bias tool for prevalence studies developed by Hoy et al (Appendix A ) [ 22 ]. There were 9 items, and each item was judged as “low” versus “high risk of bias”.
The search results and selection process are summarised in a PRISMA flowchart (eFig. 1 ). After removing duplicates, a total of 5496 titles and abstracts were screened, including 1098 (20%) screened independently by two reviewers. Discrepancies occurred on 21 (1.9%) records of titles and abstracts, and were solved through discussion. Seventy-four full text reports were retrieved and assessed for inclusion/exclusion. Twenty-nine reports were excluded with reasons (Appendix B ) and a total of 56 studies (57 reports, two reports on the same study [ 23 , 24 ], Appendix C ) were considered eligible for inclusion.
Twenty-four studies (25 reports) reported AMD, glaucoma or DR among people with cognitive impairment or dementia [ 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 ], and 34 studies reported cognitive impairment or dementia among people with AMD, glaucoma or DR [ 41 , 43 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 ]. These included two longitudinal studies [ 41 , 43 ] reporting on both directions of the association: (1) cumulative incidence of AMD among people with dementia and cumulative incidence of dementia among AMD [ 41 ]; and (2) cumulative incidence of POAG among people with dementia and cumulative incidence of dementia among POAG [ 43 ]. Studies used four methodologies for eye diseases (Appendix D ): retinal photograph grading, clinical examination, diagnostic coding, and histopathological assessments. For cognition, studies used standard diagnostic criteria for MCI or cut-offs on cognitive screening tools. Dementia was mainly assessed according to diagnostic criteria or diagnostic coding.
Eye diseases among people with cognitive impairment or dementia
Studies were conducted in Australia [ 25 , 26 ], Canada [ 27 ], China [ 28 ], France [ 29 ], Germany [ 30 , 47 ], Greece [ 31 ], Italy [ 32 ], Japan [ 33 , 34 ], the Philippines [ 35 ], Poland [ 23 , 24 ], Singapore [ 36 ], Spain [ 37 ], Taiwan [ 38 , 39 , 40 ], the UK [ 41 , 42 , 43 , 44 ] and the USA [ 45 , 46 ], and published between 1986 and 2020 (eTable 2 ). Twenty studies (83.3% of the studies, 21 reports) were published in the decade since 2011. There were nine population-based [ 25 , 36 , 38 , 39 , 40 , 41 , 43 , 44 , 45 ], three community-based [ 29 , 37 , 47 ], 11 (12 reports) hospital-based [ 23 , 24 , 26 , 27 , 28 , 31 , 32 , 33 , 34 , 35 , 42 , 46 ], and one nursing home based [ 30 ] studies. Sixteen studies (17 reports) were cross-sectional, and eight studies were longitudinal with varied follow up times reported as a mean and standard deviation of 7.6 ± 1 [ 25 ] and 2 ± 0.4 years [ 30 ] of follow-up, at least one year of follow-up [ 41 , 43 , 47 ], or reporting that AMD or glaucoma was diagnosed before the diagnosis of dementia (length of follow-up not reported) [ 38 , 39 , 40 ].
Among people with cognitive impairment
There were no studies reporting on the incidence. Prevalence of AMD ranged from 3.9% [ 37 ] to 9.4% [ 36 ] (three studies, Fig. 1 ). There was no evidence of heterogeneity or high inconsistency between the two studies on prevalence of glaucoma ( p = 0.18, I 2 = 44.1%) [ 32 , 37 ], and the pooled prevalence was 7.7% (95% CI 4.8% to 10.6%). Among people with diabetes and cognitive impairment, prevalence of DR ranged from 20% [ 25 ] to 70.1% [ 23 , 24 ] (eight studies/nine reports). The lowest prevalence of DR (11.4%) was reported in a study where diabetes was not an inclusion criterion [ 32 ].
AMD denotes age-related macular degeneration, DM diabetes mellitus, DR diabetic retinopathy, T1DM type 1 diabetes mellitus, T2DM type 2 diabetes mellitus, UK United Kingdom. a Case selection: C community-based, H hospital-based, P population-based. All studies did prospective recruitment and cross-sectional data collection. b Population: noted for the prevalence of DR, i.e., whether it was people with T1DM and/or T2DM, or general population if without notes. c Numbers are in years, and listed as mean ± standard, or median (lower and upper interquartile). Point estimates of prevalence reported in the constituent studies are presented using squares. The area of each square is proportional to the study’s weight within each group. Population-based studies were sorted first. The prevalence values are sorted from lowest to highest, with 95% confidence intervals represented by horizontal lines for individual studies and by diamonds for pooled estimates. More details on each individual study can be found in eTable 2 .
Among people with dementia
During follow-ups of “1 year or more”, cumulative incidence of AMD and glaucoma was 0.01% [ 41 ] and 0.09% [ 43 ], respectively (Fig. 2 ). Prevalence of AMD and glaucoma ranged from 1.4% [ 38 ] to 53% [ 46 ] (five studies), and from 0.2% [ 45 ] to 25.9% [ 30 ] (11 studies), respectively. One study, in which diabetes was not an inclusion criterion, reported prevalence of DR (11%) [ 32 ].
AD denotes Alzheimer’s disease, AMD age-related macular degeneration, DR diabetic retinopathy, POAG primary open-angle glaucoma, T2DM type 2 diabetes mellitus, UK United Kingdom, USA United States of America. a Study design (three components): (1) case selection: C community-based, H hospital-based, P population-based; (2) recruitment: P prospective, R retrospective; (3) data collection: X represents cross-sectional, otherwise length of follow-up is noted. Numbers are mean ± standard deviation. “EBD” denotes the corresponding eye disease was diagnosed before the diagnosis of dementia. b Population: noted when only specific types of eye disease and/or dementia were investigated in the study; noted for the prevalence of DR, i.e., whether it was people with T2DM, or general population if without notes. c Numbers are in years, and listed as mean, mean ± standard, range, or as specified. Point estimates of prevalence reported in the constituent studies are presented using squares. The area of each square is proportional to the study’s weight within each group. Population-based studies were sorted first. The frequency values are sorted from lowest to highest, with 95% confidence intervals represented by horizontal lines for individual studies and by diamonds for pooled estimates. More details on each individual study can be found in eTable 2 .
Cognitive impairment or dementia among people with eye diseases
Studies were conducted in Australia [ 48 ], Canada [ 49 ], China [ 50 ], Denmark [ 51 , 52 ], Japan [ 53 ], Malaysia [ 54 ], the Netherlands [ 55 ], Norway [ 56 ], Singapore [ 57 , 58 ], South Korea [ 59 , 60 , 61 ], Taiwan [ 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 ], Turkey [ 70 , 71 , 72 ], the UK [ 41 , 43 , 73 ] and the USA [ 74 , 75 , 76 , 77 , 78 , 79 ], and published between 1999 and 2020 (eTable 3 ). Twenty-eight studies (82.4%) were published in the most recent decade since 2011 [ 41 , 43 , 49 , 50 , 52 , 53 , 54 , 57 , 58 , 59 , 60 , 61 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 75 , 76 , 77 , 78 , 79 ]. There were 21 population-based [ 41 , 43 , 48 , 51 , 55 , 57 , 58 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 74 , 76 , 77 , 78 ], one community-based [ 73 ], and 12 hospital-based studies [ 49 , 50 , 52 , 53 , 54 , 56 , 59 , 70 , 71 , 72 , 75 , 79 ]. Other than the frequency, a single study reported on risk factors in univariate analyses, in which higher levels of HbA1c and neuron-specific enolase, and a lower education level increased the risk of cognitive impairment among people with DR [ 50 ].
Among people with AMD
Cumulative incidence of dementia ranged from 0.3% [ 41 ] to 9.9% [ 55 ] during various follow-up periods (Fig. 3 , four studies). Prevalence of cognitive impairment and dementia ranged from 8.4% [ 48 ] to 52.4% [ 59 ] (six studies) and from 9.9% [ 74 ] to 62.6% [ 79 ] (three studies), respectively.
AD denotes Alzheimer’s disease, AMD age-related macular degeneration, MoCA Montreal Cognitive Assessment, MMSE Mini-Mental State Examination, UK United Kingdom, USA United States of America. a Study design (three components): (1) case selection: C community-based, H hospital-based, P population-based; (2) recruitment: P prospective, R retrospective; (3) data collection: X represents cross-sectional, otherwise length of follow-up is noted. Numbers are mean ± standard deviation. b Population: noted when only a specific type of AMD and/or dementia was investigated in the study. c Case definition: Turkey, 2014, Dag defined cognitive impairment as <21 on the MMSE and MoCA, respectively, and reported the prevalence rates separately. d Numbers are in years, and listed as mean, mean ± standard, or as specified. Point estimates of prevalence reported in the constituent studies are presented using squares. The area of each square is proportional to the study’s weight within each group. Population-based studies were sorted first. The frequency values are sorted from lowest to highest, with 95% confidence intervals represented by horizontal lines for individual studies and by diamonds for pooled estimates. More details on each individual study can be found in eTable 3 .
Among people with glaucoma
Incidence of dementia was reported in three studies: 2.85 per 1000 person-years among people with POAG [ 63 ], and 9.22 [ 65 ] and 11.63 [ 69 ] per 1000 person-years among people with POAG or PACG. Cumulative incidence of dementia ranged from 1.4% [ 63 ] to 32% [ 76 ] during various follow-up periods (Fig. 4 , 10 studies). Prevalence of cognitive impairment and dementia ranged from 12.3% [ 49 ] to 90.2% [ 53 ] (four studies) and from 2.5% [ 62 ] to 3.3% [ 68 ] (four studies), respectively.
AD denotes Alzheimer’s disease, PACG primary angle-closure glaucoma, POAG primary open-angle glaucoma, UK United Kingdom, USA United States of America. a Study design (three components): (1) case selection: H hospital-based, P population-based; (2) recruitment: P prospective, R retrospective; (3) data collection: X represents cross-sectional, otherwise length of follow-up is noted. Numbers are mean ± standard deviation. b Population: noted when only specific types of glaucoma and/or dementia were investigated in the study. c Numbers are in years, and listed as mean, mean ± standard, median (lower and upper interquartile), or as specified. Point estimates of prevalence reported in the constituent studies are presented using squares. The area of each square is proportional to the study’s weight within each group. Population-based studies were sorted first. The frequency values are sorted from lowest to highest, with 95% confidence intervals represented by horizontal lines for individual studies and by diamonds for pooled estimates. More details on each individual study can be found in eTable 3 .
Among people with DR
Cumulative incidence of cognitive impairment was 8.5% (Fig. 5 ) [ 58 ]. Incidence rate of dementia was reported in one study, 32.87 per 1000 person-years [ 77 ]. Cumulative incidence of dementia was 5.5% [ 78 ] and 19.2% [ 77 ] within mean follow-ups of up to 7 years [ 77 , 78 ]. There were 3.9% [ 73 ] to 77.8% [ 72 ] of people with DR having cognitive impairment (three studies), and 12.5% [ 73 ] of individuals with DR had dementia.
DMO denotes diabetic macular oedema, DR diabetic retinopathy, PDR proliferative diabetic retinopathy, T1DM type 1 diabetes mellitus, T2DM type 2 diabetes mellitus, UK United Kingdom, USA United States of America. a Study design (three components): (1) case selection: C community-based, H hospital-based, P population-based; (2) recruitment: P prospective, R retrospective; (3) data collection: X represents cross-sectional, otherwise length of follow-up is noted. Numbers are mean ± standard deviation. b Population: type of diabetes was noted, also noted when only a specific type of DR was investigated in the study. c Numbers are in years and listed as mean ± standard. Point estimates of prevalence reported in the constituent studies are presented using squares. The area of each square is proportional to the study’s weight within each group. Population-based studies were sorted first. The frequency values are sorted from lowest to highest, with 95% confidence intervals represented by horizontal lines for individual studies and by diamonds for pooled estimates. More details on each individual study can be found in eTable 3 .
Associations between eye diseases and cognitive impairment or dementia
One study reported that people with dementia were more likely to have prior neovascular AMD than controls, adjusted OR 1.37 (95% CI 1.14 to 1.65) [ 38 ]. Conversely, the associations between AMD, glaucoma, or DR, and cognitive impairment or dementia have been reported in multivariable adjusted models in nine, 10, and three studies, respectively (eFigs. 2 – 4 ). In three, eight, and two longitudinal studies, pooled RRs/HRs were 1.46 (95% CI 1.31, 1.61), 1.20 (1.02 to 1.42) and 1.29 (95% CI 1.15, 1.45) for AMD, glaucoma, and DR, respectively.
Risk of bias
In 48 out of the 56 studies (86%), the target population was considered not representative of the national population with AMD, glaucoma, DR, cognitive impairment or dementia, due to the use of specific inclusion and exclusion criteria (eTable 4a–n ), e.g. exclusion of people with a history of cerebrovascular events [ 27 , 64 , 72 , 73 ], hearing impairment [ 26 , 28 , 75 ], or not living independently [ 26 , 29 ]. Among the 16 studies reporting incidence [ 41 , 43 , 51 , 52 , 55 , 58 , 60 , 61 , 63 , 64 , 65 , 67 , 69 , 76 , 77 , 78 ], only four reported all three of the relevant components, i.e., number of incident cases, person-years of follow-up, and incidence rate [ 63 , 65 , 69 , 77 ]. Only 21 (22 reports) out of 40 studies reporting on the prevalence reported on all three of the relevant components, i.e., numerator, denominator and prevalence rate [ 23 , 24 , 26 , 27 , 28 , 30 , 31 , 33 , 34 , 37 , 38 , 39 , 40 , 48 , 57 , 62 , 66 , 70 , 71 , 72 , 73 , 79 ].
Our work comprehensively reviewed the frequency of coexistent eye disease and cognitive impairment or dementia. The included studies were conducted in 21 countries or regions in Asia (23 studies), Australia (3 studies), Europe (19 studies/20 reports), and North America (11 studies). Most of the studies were conducted in high income countries, with only 13% in upper (6 studies) or lower middle (1 study) income countries. We found heterogeneity across studies with varied frequencies, which was likely due to case mix, e.g., country and ethnicity, various diagnostic criteria or definitions for eye disease and cognitive impairment or dementia, and cross-sectional versus longitudinal study design with various length of follow-up.
Potential mechanisms influencing the coexistence of eye disease and cognitive impairment
There are several potential mechanisms which have been put forward to explain relationships between eye disease and cognitive function. Whilst a full review of these mechanisms is beyond our systematic summary of the reported levels of co-existence, within the field, we highlight some of the most prominent theories. One such theory is the “use it or lose it” hypothesis in cognitive aging, i.e., a lack of, or reduction in, cognitive, physical, and social activities due to visual impairment has negative consequences for future cognitive function.
Alongside this there may also be common mechanisms operating in eye and cognitive outcomes, e.g., accumulation of similar molecules (for example amyloid β) and pathophysiology, related to both retinal changes and endothelial dysfunction in retinal and cerebral micro-vessels. Besides amyloid β, other molecules that have been found in both drusen and AD plaques include tau protein, proteoglycan, and complement component 3, etc [ 14 ]. Chronic inflammation including complement activation, oxidative stress, increased vascular endothelial growth factor in the retinal pigment epithelium and in the cerebrospinal fluid, and decreased clearance of amyloid β have also been suggested as common drivers for AMD and AD [ 14 ]. Further, similar retinal changes have been observed in glaucoma and dementia, e.g., decreased retinal thickness, protein deposits, microglial activation, neurodegeneration, and apoptosis [ 19 , 30 ]. Potential mechanisms also link diabetes and cognitive impairment including a role of the insulin-degrading enzyme (IDE), degrading amyloid β such that amyloid β aggregates in patients with diabetes and hyperinsulinemia as result of lower availability of the IDE [ 21 ]. Additionally, in the retina of people with diabetes, micro-vessels are impaired through endothelial dysfunction caused by glycation, oxidative stress, and increased polyol pathway activity, while endothelial dysfunction in the brain affects the development and progression of cerebral small vessel disease associated with the risk of cognitive impairment [ 21 ].
Why knowledge of the co-existence is important
In the current systematic review, population-based data on prevalence were sparse, and estimations were close to, if not lower than, those reported in general populations [ 2 , 4 , 11 , 12 , 13 ]. Thus our summary of the current data does not support population-based based screening of eye diseases in people with cognitive impairment or dementia, or screening of cognitive impairment or dementia in people with AMD, glaucoma, or DR. Indeed, we acknowledge the variations in prevalence estimates for each disease in general populations due to disparities in diagnostic criteria, information sources, and assessment years, etc. For instance, around 11%, 3.2%, and 1.7% Australians aged 55 years and over were affected by AMD, glaucoma, DR, respectively [ 80 ], and 8.3% of Australians aged 65 and over had dementia [ 81 ], which are slightly different to other estimations [ 2 , 4 , 11 , 12 , 13 ]. Thus, comparisons to rates in general populations should be interpreted with caution.
We did observe that co-existence tended to be more frequent in hospital- or nursing-home based settings potentially because hospital- or nursing-home based populations may be those with more co-morbidities and severe disease, or those who are more likely to seek medical advice from specialists [ 82 ]. It is important that clinicians remain alert to the potential need for an eye or cognitive assessment for their older patients. Furthermore, individuals with an eye disease, cognitive impairment, or dementia may be disadvantaged, potentially due to the challenges faced by people who rely on carers and additional help to schedule and attend optometrist appointments (for example, individuals with diabetes who had dementia were 15% less likely to receive an annual eye examination than those without dementia [ 83 ]). Therefore, preventative eye checks (or cognitive screening) might be recommended when people with cognitive impairment or dementia (or people with an eye disease) attend their check-ups.
Measures of the association
Two recent systematic reviews and meta-analyses examined whether AMD, glaucoma and/or DR increase the risk of cognitive decline and/or dementia, and vice versa [ 84 , 85 ], but the presented evidence is both sparse and mixed. A meta-analysis in 2021 found no evidence for the associations between AMD or glaucoma and risk of dementia [ 84 ], but an increased risk of dementia associated with DR, HR 1.34 (95% CI 1.11 to 1.61, pooled estimation of four studies with heterogeneity, p = 0.002) [ 84 ]. Another meta-analysis in 2019 found that individuals with dementia were at risk of AMD, pooled adjusted OR 1.24 (95% CI 1.04 to 1.47) based on four cross-sectional or case-control studies [ 85 ]. Conversely, AMD was also associated with increased risk of cognitive impairment, pooled adjusted OR 2.42 (95% CI 1.06 to 5.56) based on two cross-sectional studies [ 85 ]. However, when combining two longitudinal cohort studies with heterogeneity ( p = 0.01), the association for AMD as a risk factor for AD did not exist, pooled adjusted risk ratio 1.27 (95% CI 0.53 to 3.04) [ 85 ]. The current study added to the literature regarding the associations between eye diseases and cognitive impairment or dementia. Longitudinal research is still needed to clarify the causative relationships between eye and cognitive conditions.
Limitations
Firstly, the validity of the AMD, glaucoma, and DR diagnosis in patients with cognitive impairment or dementia may be questionable, as ocular structural and functional results may be confounded by the presence of comorbidity, such as the likely affected patient cooperation during imaging or visual field testing. Conversely, AMD, glaucoma and DR driven visual impairments may also interfere with cognitive tests, especially when studies adopted cognitive assessment scales containing vision-dependent items to define cognitive impairment. Validated adapted versions of scales, e.g., MMSE [ 86 ] and MoCA [ 87 ], could be advocated when participants or part of them were visually impaired. However, out of the nine included studies defining cognitive impairment using cut-offs on MMSE or MoCA, an adapted version had been used in only a couple [ 48 , 49 ].
Secondly, the current data is limited with less than half of the studies being population-based, and only half being longitudinal. Although many studies reported on incident cases did have cumulative incidence data available, incidence rates were available in only four studies. Further, evidence on the risk factors of the comorbidity is sparse, and thus we cannot comment on among those with one condition who are vulnerable to have another. Finally, based on the “use it or lose it” theory and biological associations between eye diseases and cognition, it can be assumed that co-existence would be more pronounced among individuals with severe disease compared to those with mild disease. Also, such coexistence is likely to increase with age, because of the increased prevalence of AMD, POAG, DR, and cognitive impairment or dementia with ageing [ 2 , 4 , 11 , 12 , 13 ]. However, current data are insufficient to explore these further.
Conclusions and implications
Our review of the co-existence of eye disease and cognitive impairment or dementia provides an important in-depth addition to the evidence base on the frequencies and confirmed the concurrence. We advocate the need for awareness of the comorbid conditions, which deserves appropriate collaborative care across disciplines. Further studies are warranted to collect data on the population-based prevalence and incidence of coexistent eye disease and cognitive impairment or dementia. Our study supports consideration of regular eye examinations or cognitive screening in clinical practice guidelines among older adults with one of these conditions.
What is known about this topic
There may be relationships between age-related macular degeneration (AMD), glaucoma or diabetic retinopathy (DR) and cognitive impairment or dementia.
What this study adds
56 studies were synthesized.
Frequencies of co-morbid AMD, glaucoma or DR and cognitive impairment or dementia were quantified.
More research is required to support or oppose regular eye examinations and cognitive screening among older adults with one of these conditions.
Data availability
The datasets generated during and/or analysed during the current study are available from the corresponding author on reasonable request.
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This study was funded and supported by University of New South Wales Ageing Futures Institute seed grants 2020. The funder had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication. Open Access funding enabled and organized by CAUL and its Member Institutions.
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Xu, Y., Phu, J., Aung, H.L. et al. Frequency of coexistent eye diseases and cognitive impairment or dementia: a systematic review and meta-analysis. Eye (2023). https://doi.org/10.1038/s41433-023-02481-4
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Dementia risk higher for elite soccer players, study finds
Alzheimer's disease and dementia were 62% more common among soccer players.
This is a MedPage Today story .
Men who played elite soccer were more likely to develop neurodegenerative diseases -- notably, dementia -- as they aged, a study in Sweden showed.
The risk of neurodegenerative disease was 46% higher among soccer players who played in the Swedish top division than in the general population, according to Dr. Peter Ueda of the Karolinska Institute in Stockholm and co-authors.
Alzheimer's disease and dementia were 62% more common among soccer players than controls, the researchers reported in Lancet Public Health.
MORE: Mediterranean diet may reduce risk of dementia, study finds: What to know about the diet
Goalkeepers did not have an increased risk of neurodegenerative disease but outfield players did, suggesting repetitive hits from heading the ball may be a factor.
"In contrast to outfield players, goalkeepers rarely head the ball," Ueda told MedPage Today. "Although other factors that differ by [soccer] player position could also affect this difference, the finding lends support to the hypothesis that heading the ball may increase the risk of dementia."
A previous study in Scotland showed that neurodegenerative disease mortality among former professional soccer players was about 3.5 times higher than the general population.
More recently, the Scotland research team reported that neurodegenerative disease risk in former soccer players was associated with field position and career length, indicating a higher risk with cumulative exposure to outfield positions.
"The fact that this well-conducted study replicates prior research on [soccer] players in Scotland should convince skeptics that the connection between heading and dementia is real and preventable," said Chris Nowinski of the Concussion Legacy Foundation in Boston, who wasn't involved with the study.
"We need to take steps to minimize risk by increasing the age at which children begin heading, and then take steps to reduce the frequency and magnitude of headers," Nowinski told MedPage Today.
"The Football Association in England is leading the conversation on age of first exposure by eliminating heading before age 12," Nowinski pointed out.
MORE: LA assisted living facility faces felony charges over deadly COVID-19 outbreak
"Other countries should match that policy, and I anticipate the age will increase as people begin to realize the benefits of fewer concussions in children and CTE (chronic traumatic encephalopathy) cases in [soccer] players," he added. "Once heading is introduced, sports organizations need to set strict limits, especially on higher magnitude impacts."
Ueda's research team studied health records of 6,007 male soccer players who played in the Swedish top division Allsvenskan from 1924 through 2019, comparing them with 56,168 matched controls from the general Swedish population.
Over an average follow-up time of 28 years, 8.9% of elite soccer athletes and 6.2% of controls were diagnosed with neurodegenerative disease. A total of 8.2% of soccer players developed Alzheimer's disease or dementia, compared with 5.1% of men in the general population.
The risk of motor neuron disease, including amyotrophic lateral sclerosis (ALS), was similar among players and non-players. Parkinson's disease was less common among soccer players than the general population, and death from any cause was slightly lower.
The lower overall mortality could indicate that elite soccer players have better overall health and physical fitness than the general population, said study co-author Dr. Björn Pasternak, also of the Karolinska Institute.
MORE: New data shows Alzheimer's drug can slow cognitive decline
"Physical activity is associated with a lower risk of dementia, so it could be hypothesized that the potential risks from head impacts are being somewhat offset by having good physical fitness," Pasternak said. "Good physical fitness may also be the reason behind the lower risk of Parkinson's disease."
The research shows an association between dementia and elite soccer, not cause-and-effect, Ueda emphasized.
"Even if we would have perfect data on causality, what to do with it is a matter of values and a decision for the broader community and individual players to make," he said. "Our study provides data that could support such decision-making."
"I think it is important to emphasize that these findings are based on elite players who were active mostly during the mid-20th century," Ueda added. "Their applicability to contemporary elite players and to amateur and youth players is uncertain."
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New Study Finds These 2 Diets Can Reduce Risk of Alzheimer’s
The MIND and Mediterranean diets are linked to healthier brains.
- New research links two popular diets to a lowered risk of Alzheimer’s disease.
- People who most closely followed the diets had less tangles and plaques in their brains.
- Experts say the findings are promising, but more research is needed.
Alzheimer’s disease is a complicated condition, and experts are still trying to figure out why some people develop it while others don’t. Now, a new study suggests that what you eat can play a role in your risk of developing Alzheimer’s—and two diets in particular may help lower your chances of developing the devastating disease.
The study, which was published in the journal Neurology , examined the brains of more than 580 people who donated their body to Rush University’s Memory and Aging Project , which has been collecting annual dietary information and doing annual check-ups on study participants since 2004. The study analyzed data on the dietary habits of participants from 2014 through 2020 or 2021, and compared that with the number of plaques and tangles that were in each person’s brain during an autopsy.
Plaques and tangles, in case you’re not familiar with them, are key markers of Alzheimer’s disease. In a person who has Alzheimer’s disease, beta-amyloid proteins clump together to form plaques that collect between neurons and interfere with cell function, according to the National Institute on Aging (NIA). Tangles are an accumulation of a protein called tau that collect inside neurons and interfere with communication between neurons, the NIA says.
The researchers discovered that people who had eating patterns that closely followed the MIND or Mediterranean diets had almost 40% lower chances of developing Alzheimer’s disease than others.
The researchers specifically found that green leafy vegetables were the most beneficial, with brain tissue from people who ate the most leafy greens looking nearly 19 years younger in terms of plaque buildup than those who only had one or less servings of leafy greens a week.
The study raises a lot of questions about diet’s role in Alzheimer’s disease, as well as why these eating plans in particular may be helpful in lowering your risk. Here’s the deal.
How can diet impact a person’s Alzheimer’s risk?
There are a lot of potential factors that can influence your risk of developing Alzheimer’s disease, including genetics and aging, the NIA says. As for diet, the National Institutes of Health (NIH) says that it’s possible that what you eat may influence your risk of developing Alzheimer’s disease. The NIH also points to the MIND and Mediterranean diets as being especially helpful in the prevention of Alzheimer’s disease.
“We and others previously found that healthy diets are associated with reduced dementia risk and better cognitive function in an aging population,” says lead study author Puja Agarwal, Ph.D., an assistant professor of internal medicine at the Rush University Medical Center in Chicago. What the latest study shows is that diet may be directly related to the formation of plaques and tangles in the brain, Agarwal says.
“The exact mechanism of how diet and plaques and tangles relate needs further investigation and we speculated that there might be other mechanisms through which diet may impact the risk for Alzheimer’s disease,” she says.
And, at a basic level, you are what you eat, says Amit Sachdev, M.D., M.S., medical director in the Department of Neurology at Michigan State University. “Diet is a metric for overall wellness,” he says. “In general. healthy body means healthy brain.”
Why might the MIND and Mediterranean diets lower your risk of developing Alzheimer’s?
Again, this is still being explored. However, there are some theories.
“One of the proposed mechanisms is that both the MIND and the Mediterranean are plant-based diets rich in various essential nutrients and bioactive compounds that are required to maintain brain health,” Agarwal says. “They also have antioxidant and anti-inflammatory properties which may help prevent amyloid burden and neuronal loss.”
Dr. Sachdev agrees that the diets’ anti-inflammatory properties may play a role. “Some diets are better at controlling body-wide inflammation,” he says. “Unfortunately, the typical starch-heavy American diet is not a great choice.” However, he says, the Mediterranean and MIND diets “balance styles of food and portion size in a way that reduces overall burden of body inflammation.”
Dr. Sachdev also notes that the Mediterranean diet in particular is linked to blood vessel health. “When we think of Mediterranean diet, we think of the health of blood vessels in the brain and reducing strokes. There is strong evidence for this,” he says. Research has also found that blood vessel issues are linked to an increased risk of Alzheimer’s.
Mediterranean diet basics
The Mediterranean diet is based on the lifestyles of people who live in the Mediterranean region, which includes Greece, Italy, and Spain, explains Jessica Cording, R.D., author of The Little Book of Game-Changers . It focuses on high intakes of vegetables, legumes, fruits, nuts, grains, fish, seafood, extra virgin olive oil, and some red wine. The diet also encourages followers to limit red meat, Cording says.
“The Mediterranean diet is designed to be a lifestyle,” Cording says, noting that people on the diet are also encouraged to be active. Research has linked the Mediterranean diet with good heart health , optimal blood sugar levels , and a lowered risk of dementia .
MIND diet basics
The MIND diet (which stands for Mediterranean–DASH Intervention for Neurodegenerative Delay) is a form of the Mediterranean diet that focuses on plant-based foods linked to dementia prevention, according to the NIA . It specifically encourages people to eat from these food groups:
- Leafy green vegetables, at least six servings/week
- Other vegetables, at least one serving/day
- Berries, at least two servings/week
- Whole grains, at least three servings/day
- Fish, one serving/week
- Poultry, two servings/week
- Beans, three servings/week
- Nuts, five servings/week
- Wine, one glass/day
The diet also recommends that you limit servings of red meat, sweets, cheese, butter and margarine, and fast and fried foods, the NIA says.
What does this mean for your diet?
If you’re concerned about your Alzheimer’s disease risk, experts say it’s definitely worth taking a look at your diet. However, it’s important to stress that diet isn’t the only factor in the development of Alzheimer’s disease.
“Alzheimer’s disease risk is greatly influenced by genetics and age. Diet is a part of the conversation,” Dr. Sachdev says.
If you want to change up your diet but are uncertain where to start, Agarwal recommends keeping in mind basic principles of both the MIND and Mediterranean diets. Both diets “emphasize consuming more vegetables, especially green leafy, fruits including berries, whole grains, legumes, nuts, poultry, fish, and olive oil,” Agarwal says. “These diets also encourage avoiding or limiting high-fat, high-sugar foods, including red meat, fried foods, butter, full-fat cheese, and pastries and sweets.”
Not sure where to start? Try “incorporating more whole plant foods into your diet,” says Molly Rapozo , R.D.N., senior nutrition and health educator at Pacific Neuroscience Institute in Santa Monica, Calif. “If leafy greens aren’t a staple already, this could be a great place to start,” she says.
And, if you want to improve your diet but aren’t sure how to make changes work for you, Cording suggests that you consider meeting with a registered dietitian. They can help guide you on foods and meals to try to get you on the right track.
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Therapeutic inhalation of hydrogen gas for alzheimer’s disease patients and subsequent long-term follow-up as a disease-modifying treatment: an open label pilot study.
1. Introduction
2.1. hydrogen treatment improved ad as assessed by adas-cog, 2.2. improvement of neurons by h 2 inhalation as assessed by diffusion tensor imaging, 3. discussion, 4. materials and methods, 4.1. approval for this study, 4.2. patient selection, 4.3. collection of data from untreated control patients, 4.4. treatment, 4.5. adas-cog examination, 4.6. measurement of the integrity of neurons by diffusion tensor imaging, 4.7. statistical analysis, 5. conclusions, author contributions, institutional review board statement, informed consent statement, data availability statement, acknowledgments, conflicts of interest.
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Share and Cite
Ono, H.; Nishijima, Y.; Ohta, S. Therapeutic Inhalation of Hydrogen Gas for Alzheimer’s Disease Patients and Subsequent Long-Term Follow-Up as a Disease-Modifying Treatment: An Open Label Pilot Study. Pharmaceuticals 2023 , 16 , 434. https://doi.org/10.3390/ph16030434
Ono H, Nishijima Y, Ohta S. Therapeutic Inhalation of Hydrogen Gas for Alzheimer’s Disease Patients and Subsequent Long-Term Follow-Up as a Disease-Modifying Treatment: An Open Label Pilot Study. Pharmaceuticals . 2023; 16(3):434. https://doi.org/10.3390/ph16030434
Ono, Hirohisa, Yoji Nishijima, and Shigeo Ohta. 2023. "Therapeutic Inhalation of Hydrogen Gas for Alzheimer’s Disease Patients and Subsequent Long-Term Follow-Up as a Disease-Modifying Treatment: An Open Label Pilot Study" Pharmaceuticals 16, no. 3: 434. https://doi.org/10.3390/ph16030434
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In this case study, we describe the symptoms, neuropsychological testing, and brain pathology of a man with Alzheimer's disease (AD). AD commonly presents with impairment of memory and language function. In this case, language difficulties were noted more prominently than was memory impairment. Throughout the limbic system and neocortex of ...
Over an average follow-up time of 28 years, 8.9% of elite soccer athletes and 6.2% of controls were diagnosed with neurodegenerative disease. A total of 8.2% of soccer players developed Alzheimer ...
Alzheimer's disease is a complicated condition, and experts are still trying to figure out why some people develop it while others don't. Now, a new study suggests that what you eat can play a ...
The objective of this study was to investigate how a measure of educational and occupational attainment, a component of cognitive reserve, modifies the relationship between biomarkers of pathology and cognition in Alzheimer's disease. The biomarkers evaluated quantified neurodegeneration via atrophy on magnetic resonance images, neuronal injury via cerebral spinal fluid t-tau, brain amyloid ...
(1) Background: Alzheimer's disease (AD) is a progressive and fatal neurodegenerative disorder. Hydrogen gas (H2) is a therapeutic medical gas with multiple functions such as anti-oxidant, anti-inflammation, anti-cell death, and the stimulation of energy metabolism. To develop a disease-modifying treatment for AD through multifactorial mechanisms, an open label pilot study on H2 treatment ...