Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 5,209 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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A Clinical Task Force, composed of clinical leaders from Alzheimer's Disease Centers (ADC), was convened by the National Institute on Aging to develop a uniform set of assessment procedures to characterize individuals with mild Alzheimer disease and mild cognitive impairment in comparison with nondemented aging.
Why it matters
Describes the Uniform Data Set, a common set of clinical and cognitive assessments that a National Institute on Aging task force developed for Alzheimer's Disease Centers to collect over time on people with mild Alzheimer disease, mild cognitive impairment and nondemented aging. The data go to the National Alzheimer's Coordinating Center to support shared research.
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Cortical thickness is a more reliable measure of atrophy than volume due to the low variability in the cytoarchitectural structure of the grey matter.
Why it matters
This study found that cortical thinning began in the medial temporal lobe and some frontal and parietal regions in mild cognitive impairment, and spread more widely as the disease progressed to Alzheimer's disease. This describes a pattern of brain change, but it does not test any treatment, cure, or prevention.
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These results may lead to a new avenue of inquiry in the prevention of Alzheimer's disease.
Why it matters
In this cohort of Japanese Americans, drinking fruit and vegetable juices at least three times per week was associated with a lower hazard ratio for probable Alzheimer's disease compared with drinking them less than once per week. The authors say the results may lead to a new avenue of inquiry in prevention.
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Beta amyloid is one of the major histopathological hallmarks of Alzheimer's disease.
Why it matters
16 people with Alzheimer's were rescanned about 2 years later. Amyloid on PiB scans did not change significantly while brain glucose use fell by 20%, which the authors suggest means amyloid buildup reaches a plateau by early clinical stages and may come before declines in metabolism and thinking.
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51/100
Vascular risk factors for Alzheimer disease (AD) and vascular dementia (VaD) have been evaluated; however, few studies have compared risks by dementia subtypes and sex.
Why it matters
In 3,264 Cache County residents aged 65 or older, a past stroke was linked to a much higher risk of vascular dementia in both women (aHR 16.90) and men (aHR 10.95). Obesity was linked to Alzheimer's disease (aHR 2.23) and diabetes to vascular dementia (aHR 3.33) in women only, while self-reported high blood pressure and cholesterol were not linked to Alzheimer's after adjustment. The risk factors were self- or proxy-reported and the study is observational, so it shows associations that differ by sex, not that managing these factors prevents dementia.
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APOE genotype strongly predicts the rate of cognitive decline in Alzheimer disease.
Why it matters
Using a nonlinear model, having an APOE epsilon4 allele was linked to earlier and faster cognitive decline in Alzheimer's disease, while an epsilon2 allele was linked to slower decline. This helps predict how the disease may progress in individuals but does not treat or prevent it.
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In the Cardiovascular Health Cognition Study, consumption of fatty fish was associated with a reduced risk of dementia and Alzheimer disease for those without the APOE epsilon4 allele.
Why it matters
In the Cardiovascular Health Cognition Study, people who reported eating fatty fish (such as tuna) more than twice a week had a 41% lower risk of Alzheimer disease than those eating fish less than once a month (95% CI 0.36 to 0.95). The 28% lower risk of any dementia was less certain, because its interval (0.51 to 1.02) includes no effect. The link was "selective to those without the epsilon4 allele," lean fried fish showed "no protective effect," and adjusting for education and income weakened the result, so this is an association and does not show that fish prevents dementia.
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Alzheimer disease (AD) and, to a lesser extent, dementia with Lewy bodies (DLB) showed more pronounced MTA.
Why it matters
This imaging study found that medial temporal lobe atrophy was seen even in cognitively intact people with Parkinson disease and was not more pronounced in Parkinson disease dementia, while Alzheimer disease showed more pronounced atrophy. It compares brain structure across disorders and does not test any treatment, cure, or prevention.
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Increased annual atrophy rate in the medial temporal lobe is a potential diagnostic marker of the progression of Alzheimer disease.
Why it matters
In 18 patients with a known date of Alzheimer disease onset, the annual rate of medial temporal lobe atrophy correlated with time since onset, and this measure classified Alzheimer disease versus normal cognition with 92.3% accuracy. This is about a potential diagnostic marker of disease progression, not a treatment, cure or prevention for Alzheimer's disease.
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In cross-section and longitudinally, our results show that evaluations of the P-tau231 level are highly correlated with reductions in the MRI hippocampal volume and by using CSF and MRI measures together one improves the separation of NL and MCI.
Why it matters
This study found that P-tau231 levels correlated with reductions in MRI hippocampal volume, and that combining MRI and cerebrospinal fluid measures improved separation of normal and mild cognitive impairment groups. The authors conclude that combined MRI and cerebrospinal fluid measures incrementally contribute to early diagnosis and monitoring, not to treatment or cure.
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The study aimed at mapping (i) the distributed electroencephalographic (EEG) sources specific for mild Alzheimer's disease (AD) compared to vascular dementia (VaD) or normal elderly people (Nold) and (ii) the distributed EEG sources sensitive to the mild AD at different stages of severity.
Why it matters
This EEG study mapped cortical rhythms in mild Alzheimer's disease compared with vascular dementia and normal elderly people. It is a diagnostic mapping study and does not test any treatment, cure or prevention.
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The number of persons with AD in the US population will continue to increase unless new discoveries facilitate prevention of the disease.
Why it matters
Using incidence data from a Chicago community study applied to US Census projections, the authors estimated 4.5 million people with Alzheimer disease in the US in 2000, rising to 13.2 million by 2050. Much of the projected growth was among people aged 85 and older.
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51/100
Serum hypercholesterolemia may be an early risk factor for the development of AD amyloid pathology.
Why it matters
In this autopsy study, higher cholesterol was linked to amyloid deposition in the youngest subjects aged 40 to 55, but this difference disappeared in older subjects. It suggests cholesterol may matter early, but it does not show that lowering cholesterol prevents Alzheimer disease.
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Dietary intake of n-3 fatty acids and weekly consumption of fish may reduce the risk of incident Alzheimer disease.
Why it matters
Followed 815 residents aged 65 to 94 for an average of 3.9 years, during which 131 developed Alzheimer's disease. Those who ate fish once a week or more had 60% less risk than those who rarely or never ate fish in an adjusted model, and the authors say dietary n-3 fatty acids and weekly fish may reduce the risk of Alzheimer's disease.
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Measurement of HL plasma levels may have potential usefulness as an adjunct in monitoring treatment response to oral HL in AD patients with psychosis or disruptive behavior.
Why it matters
In this 6-week trial of 71 outpatients with Alzheimer's disease, haloperidol plasma levels correlated with clinical efficacy on several measures and with extrapyramidal side effects, while oral dose did not. It concerns monitoring an antipsychotic used for psychosis and behavioral symptoms, not treating, curing or preventing Alzheimer's disease itself.
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Clinicopathologic data from 285 autopsies were analyzed.
Why it matters
In 285 autopsies of long-standing Honolulu-Asia Aging Study participants, 118 of whom had definite or probable dementia, the study sorted each brain by its dominant microscopic pathology. Microvascular lesions dominated in 14% of decedents, Alzheimer lesions in 12%, hippocampal sclerosis and cortical Lewy bodies in 5% each, and 9% showed two or more processes together. The stored summary does not report how these groups related to dementia, and this descriptive autopsy study tests no treatment or prevention.
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The visual association test (VAT) is a brief learning task based on imagery mnemonics.
Why it matters
This brief learning task was tested to see whether it can tell apart people with early dementia of the Alzheimer type from people without dementia. It is a diagnostic test only, so it does not treat, cure or prevent Alzheimer's disease.
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Although it is clear that apoE plays an important role in the genetics of late-onset Alzheimer disease (AD), evidence exists that additional genes may play a role in AD, and estimates of the total contribution of apoE to the variance in onset of AD vary widely.
Why it matters
This segregation analysis of families with late-onset Alzheimer disease estimated that four additional loci contribute to variation in age at onset, with contributions similar to or greater than that of apoE. The results suggest several not-yet-localized genes may play a larger role than apoE, but no treatment or cure is offered.
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Nicotine is a cholinergic agonist that acts, not only post-synaptically, but also releases pre-synaptic acetylcholine, and in animal models has been shown to reverse spatial memory decline in rats with lesion in the medial septal nucleus and to show recovery on memory in aged monkeys.
Why it matters
This review aimed to assess nicotine for Alzheimer's disease but found the trials were of poor quality and could not be combined. It provides no evidence that nicotine treats or prevents the disease, and notes serious adverse effects such as cardiovascular risks in elderly people.
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We studied CSF-tau and CSF-Abeta42 in 16 patients with mild cognitive impairment (MCI) who at follow-up investigations 6-27 months later had progressed to Alzheimer's disease (AD) with dementia.
Why it matters
In 16 patients with mild cognitive impairment who later progressed to Alzheimer's disease, 14 had high CSF-tau and/or low CSF-Abeta42 levels at baseline. The authors say these markers are abnormal before the onset of clinical dementia and may help identify mild cognitive impairment patients who will develop Alzheimer's disease.
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51/100
Why it matters
Examines soluble amyloid β peptide concentration as a predictor of synaptic change in Alzheimer's disease.
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The sensitivity of CSF-beta-amyloid(1-42) level as a diagnostic marker for AD is high.
Why it matters
In this 20-month follow-up of 53 people with Alzheimer's disease and 21 healthy people of similar age at one Swedish hospital, the authors concluded that the level of beta-amyloid(1-42) in spinal fluid had "high" sensitivity as a diagnostic marker, varied little within the same patient over time, and was low even "in the earlier stages of dementia". Our copy of the abstract has lost its results figures, so no sensitivity, specificity or level values can be shown here, and the stated questions about ApoE and early- versus late-onset disease have no reported answer. It is a test-measurement study: it does not show that amyloid causes the disease or that any treatment works.
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The histopathologic changes distinguishing early Alzheimer disease (AD) from normal or pathologic aging are not clearly defined.
Why it matters
Autopsies of 59 elderly, well-educated volunteers who showed no cognitive impairment on testing found that many had abundant senile plaques and/or neurofibrillary tangles, and only 17% had no or few degenerative brain changes. This shows that Alzheimer-type brain changes can be present in people who are not cognitively impaired, which complicates distinguishing early Alzheimer's disease from normal aging.
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51/100
The most proximal brain events associated with the clinical expression of dementia are progressive neuronal dysfunction and loss of neurons in specific regions of the brain.
Why it matters
This paper states that the most proximal brain events associated with the clinical expression of dementia are progressive neuronal dysfunction and loss of neurons in specific regions of the brain. It does not report any treatment, cure, or prevention findings.
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Anti-inflammatory drugs have been suggested as a possible treatment for Alzheimer's disease (AD).
Why it matters
This postmortem comparison of nondemented arthritic patients with chronic NSAID use and nondemented controls examined whether NSAIDs modify Alzheimer-type pathology. It reports no treatment, cure, or prevention for Alzheimer's disease.
From across this topic
10 of the 5,172 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Cerebrospinal fluid biomarkers for understanding multiple aspects of Alzheimer's disease pathogenesis
- Harnessing peripheral DNA methylation differences in the Alzheimer's Disease Neuroimaging Initiative (ADNI) to reveal novel biomarkers of disease
- Prevalence and Outcomes of Amyloid Positivity Among Persons Without Dementia in a Longitudinal, Population-Based Setting
- An unbiased approach to identifying tau kinases that phosphorylate tau at sites associated with Alzheimer disease
- Psychiatric symptoms vary with the severity of dementia in probable Alzheimer's disease
- Brain organoids in Alzheimer disease and related tauopathies: Challenges and opportunities for translational readiness
- Oxidative damage is the earliest event in Alzheimer disease
- Longitudinal changes in white matter disease and cognition in the first year of the Alzheimer disease neuroimaging initiative
- Ambroxol as a Treatment for Parkinson Disease Dementia: A Randomized Clinical Trial
- Ophthalmic imaging and artificial intelligence in early diagnosis of Alzheimer disease