28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Understanding the lifetime risk of dementia can inform public health planning and improve patient engagement in prevention. 1 key finding →
Design: cohort Participants: 15,043 Evidence: high
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Plasma biomarkers of AD neuropathology, neuronal injury, and astrogliosis increase with age and are associated with known dementia risk factors. 5 key findings →
Design: cohort Participants: 1,525 Evidence: high
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Dementia and MCI are associated with neuropsychiatric symptoms in clinical samples. 4 key findings →
Design: cohort study Participants: 138 Evidence: moderate
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An increasing number of midlife vascular risk factors was significantly associated with elevated amyloid SUVR; this association was not significant for late-life risk factors. 5 key findings →
Design: cohort study Participants: 20 Evidence: moderate
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Among 34 349 participants, 26 088 who self-reported Black or White race, were free of stroke and dementia, and had covariate data at or before the first cognitive assessment were included for analysis. 2 key findings →
Design: cohort study Participants: 349 Evidence: moderate
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Midlife vascular risk factors are associated with increased risk of dementia in black and white ARIC Study participants. 4 key findings →
Design: prospective cohort Participants: 744 Evidence: moderate
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We tested the hypothesis that plasma neurofilament light chain (NfL) identifies asymptomatic carriers of familial frontotemporal lobar degeneration (FTLD)-causing mutations at risk of disease progression. 4 key findings →
Design: longitudinal study Participants: 277 Evidence: moderate
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Of 200 participants, 99 were assigned to methylphenidate and 101 to placebo. 5 key findings →
Design: longitudinal study Participants: 200 Evidence: high
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We found that distinct sphingolipid species including sphingomyelin (SM) with acyl residue sums C16:0, C18:1, and C16:1 (SM C16:0, SM C18:1, SM C16:1) and hydroxysphingomyelin with acyl residue sum C14:1 (SM (OH) C14:1) were consistently associated with severity of AD pathology at autopsy and AD progression across prodromal and preclinical stages. 5 key findings →
Design: longitudinal study Participants: 44 Evidence: moderate
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Incidence rates for AD in the BLSA are consistent with published rates in other studies. 2 key findings →
Design: longitudinal study Participants: 1,236 Evidence: moderate
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In this study, risk of dementia significantly increased after ischemic stroke, independent of vascular risk factors. 5 key findings →
Design: prospective cohort Participants: 379 Evidence: moderate
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Older adults with CVD other than stroke had a higher risk of dementia and AD than did those without CVD. 5 key findings →
Design: cohort study Participants: 3,602 Evidence: moderate
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) is a longitudinal multisite observational study of healthy elders, mild cognitive impairment (MCI), and Alzheimer's disease. 5 key findings →
Design: longitudinal study Evidence: moderate
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After correcting for multiple comparisons using the Bonferroni procedure, we observed a statistically significant interaction between APOE-ε4 and sex on CSF total tau (β = 0.41; 95% CI, 0.27-0.55; P Conclusions and relevance We provide robust evidence of a stronger association between APOE-ε4 and CSF tau levels among women compared with men across multiple independent data sets. 5 key findings →
Design: cohort study Participants: 1,798 Evidence: moderate
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Hearing loss is independently associated with incident all-cause dementia. 4 key findings →
Design: longitudinal study Participants: 639 Evidence: moderate
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Late-life declines in blood pressure following prolonged hypertension may be associated with poor cognitive outcomes. 5 key findings →
Design: cohort study Participants: 833 Evidence: moderate
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High cholesterol in late life was associated with decreased dementia risk, which is in contrast to previous studies suggesting high cholesterol in mid-life is a risk factor for later dementia. 5 key findings →
Design: longitudinal study Participants: 392 Evidence: moderate
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Early identification of patterns of abnormality is of fundamental importance for detecting disease onset and tracking progression. 2 key findings →
Design: longitudinal study Participants: 1,017 Evidence: moderate
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Of 4467 participants who underwent 9208 longitudinal cognitive sessions, 2698 (60.4%) were female, and the mean age (SD) was 74.3 (9.2) years; 3213 were cognitively unimpaired, 972 had mild cognitive impairment, and 282 had AD dementia. 2 key findings →
Design: cohort study Participants: 4,467 Evidence: moderate
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A total of 7731 participants were included in analysis of risk factors measured at age 45 to 54 years (4494 female [58%]; 2207 Black [29%]; 5524 White [71%]), 12 274 contributed to analysis of risk factors measured at age 55 to 64 years (6698 female [55%]; 2886 Black [24%]; 9388 White [76%]), and 6787 contributed to analysis of risk factors measured at age 65 to 74 years (3764 female [56%], 1375 Black [20%]; 5412 White [80%]). 3 key findings →
Design: cohort Participants: 12,274 Evidence: moderate
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Use of naproxen or celecoxib did not improve cognitive function. 2 key findings →
Design: longitudinal study Evidence: high
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Black decedents were less likely than White decedents to use hospice for 3 or more days (132 of 378 [34.9%] vs 385 of 834 [46.2%]; P Conclusions and relevance Despite the increase in the use of hospice care in recent decades, racial disparities in the use of hospice remain, especially for noncancer deaths. 1 key finding →
Design: cohort study Participants: 1,212 Evidence: moderate
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In this community-based cohort without dementia, florbetapir uptake is associated with older age and APOE genotype. 5 key findings →
Design: longitudinal study Participants: 329 Evidence: moderate
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Use of NSAIDs was associated with a lower risk of dementia (adjusted hazard ratio or aHR 0.76, 95% CI or CI 0.60-0.96) and, in particular, AD (aHR 0.63, CI 0.45-0.88), but not VaD (aHR 0.92, CI 0.65-1.28). 3 key findings →
Design: cohort study Participants: 3,229 Evidence: moderate
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Our prospective findings provide evidence for what may be an early contributory role of systemic inflammation in neurodegeneration and cognitive aging. 3 key findings →
Design: cohort study Participants: 1,633 Evidence: moderate
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Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 28,180 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,034 records (3.7% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →