27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
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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Frequent consumption of fruits and vegetables, fish, and omega-3 rich oils may decrease the risk of dementia and Alzheimer disease, especially among ApoE epsilon 4 noncarriers. 4 key findings →
Design: cohort study Participants: 8,085 Evidence: moderate
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Over 10 years of close clinical dementia surveillance in this cohort study, loneliness was associated with increased dementia risk; this tripled in adults whose baseline risk would otherwise be relatively low on the basis of age and genetic risk, representing a majority of the US population. 5 key findings →
Design: cohort study Participants: 2,308 Evidence: moderate
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The findings of the current study show that the longitudinal, cumulative trajectory of cardiovascular risk is predictive of dementia risk and associated with the emergence of memory decline. 4 key findings →
Design: prospective cohort Participants: 1,244 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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Fasting lipid fractions (triglycerides [TGs], high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], total cholesterol [TC]) were studied as continuous variables, and results are reported per SD increase of each lipid fraction. 5 key findings →
Design: cohort study Participants: 9,294 Evidence: moderate
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Our findings suggest that statins might be associated with a lower risk of incident AD among individuals with the APOE ε4 allele. 5 key findings →
Design: cohort Participants: 4,807 Evidence: early
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The APOE epsilon4 allele is a genetic risk factor for dementia with stroke, including VaD and AD with CVD. 5 key findings →
Design: case-control study Participants: 187 Evidence: moderate
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At 48 months, group differences between clinical progressors and non-progressors were significant for self (2.13, SE=0.45, P Conclusions and relevance Demonstrating long-term clinical benefit will be critical for the success of recently launched secondary prevention trials. 1 key finding →
Design: longitudinal study Participants: 468 Evidence: moderate
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Alongside APOE ε4, iPRS-DEM may refine risk stratification for the enrichment of dementia clinical trials and prevention programs. 3 key findings →
Design: cohort Participants: 241,935 Evidence: moderate
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In white older adults, prevalent Alzheimer disease (AD) was longitudinally associated with a reduced risk of cancer, and a history of cancer was associated with a reduced risk of AD. 5 key findings →
Design: cohort study Participants: 3,020 Evidence: moderate
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Higher dietary intakes of flavonols may be associated with reduced risk of developing Alzheimer dementia. 5 key findings →
Design: prospective cohort Participants: 691 Evidence: moderate
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The 4417 participants in the study included 2618 women (59%) and had a mean (SD) age of 71.3 (4.7) years. 5 key findings →
Design: cross-sectional Participants: 2,618 Evidence: low
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Worldwide, the prevalence of dementia is increasing and diet as a modifiable factor could play a role. 3 key findings →
Participants: 493,888 Evidence: moderate
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Employing time-dependent proportional hazards modeling, the authors found no significant association between statin use and incident dementia or probable AD. 2 key findings →
Design: cohort study Participants: 312 Evidence: moderate
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Overall, cumulative incidence was uniformly higher in NACC than in the population-based cohorts. 3 key findings →
Participants: 5,073 Evidence: moderate
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During the 17-year follow-up period, 164 participants developed dementia; 136 of these cases were AD. 5 key findings →
Participants: 164 Evidence: moderate
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To evaluate reverse causation, we assessed whether a polygenic risk score for AD is associated with HGS. 5 key findings →
Design: cohort study Evidence: moderate
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During 21 046 person-years of follow-up (median follow-up, 6.3 years), 199 women developed dementia, including 159 who developed AD. 5 key findings →
Design: cohort study Participants: 3,601 Evidence: moderate
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The influence of this genetic risk may begin in early life and make an individual more susceptible to cognitive impairment in late life. 1 key finding →
Design: cohort study Evidence: moderate
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Genetic risk for AD does not modify the association between hypertension and dementia. 4 key findings →
Design: cohort Participants: 11,597 Evidence: moderate
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Our findings highlight the importance of personalized risk assessments and the development of tailored interventions based on genetic background to prevent dementia more effectively. 5 key findings →
Design: cohort Participants: 182,473 Evidence: moderate
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Smoking and education, which have opposing risk effects on AD and PD, are not risk factors for DLB; however, depression and low caffeine intake, both risk factors for AD and PD, increase risk of DLB more strongly than in either. 2 key findings →
Participants: 147 Evidence: moderate
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Mean IGF-1 levels were 144 ± 60 μg/L in generation 1 and 114 ± 37 μg/L in generation 2. 3 key findings →
Participants: 789 Evidence: low
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We systematically compared structural imaging patterns of advanced brain aging (ABA) in the general-population, herein defined as significant deviation from typical BA to those found in Alzheimer disease (AD). 5 key findings →
Participants: 2,705 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →