27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment. 4 key findings →
Design: meta-analysis Participants: 2,914 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Compared with placebo, the use of G. biloba, 120 mg twice daily, did not result in less cognitive decline in older adults with normal cognition or with mild cognitive impairment. 3 key findings →
Participants: 1,545 Evidence: high
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Two loci were identified to have genome-wide significance for the first time: rs744373 near BIN1 (odds ratio [OR],1.13; 95% confidence interval [CI],1.06-1.21 per copy of the minor allele; P = 1.59x10(-11)) and rs597668 near EXOC3L2/BLOC1S3/MARK4 (OR, 1.18; 95% CI, 1.07-1.29; P = 6.45x10(-9)). 3 key findings →
Participants: 35,000 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genome-wide significance in fully adjusted models (sex, age, APOE genotype, population stratification) was observed for a SNP in ABCA7 (rs115550680, allele = G; frequency, 0.09 cases and 0.06 controls; odds ratio [OR], 1.79 [95% CI, 1.47-2.12]; P = 2.2 × 10(-9)), which is in linkage disequilibrium with SNPs previously associated with Alzheimer disease in Europeans (0.8 Conclusions and relevance In this meta-analysis of data from African American participants, Alzheimer disease was significantly associated with variants in ABCA7 and with other genes that have been associated with Alzheimer disease in individuals of European ancestry. 4 key findings →
Design: meta-analysis Participants: 5,896 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
In this exploratory analysis, the APOE ε3[R145C] missense variant was associated with an increased risk of AD among individuals of African ancestry with the ε3/ε4 genotype. 5 key findings →
Design: case-control Participants: 31,929 Evidence: moderate
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Among Caucasian subjects from clinic- or autopsy-based studies, the risk of AD was significantly increased for people with genotypes epsilon2/epsilon4 (OR=2.6, 95% CI=1.6-4.0), epsilon3/epsilon4 (OR=3.2, 95% CI=2.8-3.8), and epsilon4/epsilon4 (OR=14.9, 95% CI= 10.8-20.6); whereas, the ORs were decreased for people with genotypes epsilon2/epsilon2 (OR=0.6, 95% CI=0.2-2.0) and epsilon2/epsilon3 (OR=0.6, 95% CI=0.5-0.8). 2 key findings →
Participants: 5,930 Evidence: low
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The presence of an APOE-epsilon4 allele is a determinant of AD risk in whites, but African Americans and Hispanics have an increased frequency of AD regardless of their APOE genotype. 2 key findings →
Design: longitudinal study Participants: 1,079 Evidence: moderate
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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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These results suggest that the inheritance of APOE epsilon 4 is associated with reduced cerebral parietal metabolism and increased asymmetry in non-demented relatives at risk for probable AD. 4 key findings →
Design: longitudinal study Participants: 12 Evidence: moderate
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Among the 286 autopsied brains of 544 participants, brain mercury levels were positively correlated with the number of seafood meals consumed per week (ρ = 0.16; P = .02). 5 key findings →
Design: cohort study Participants: 286 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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A significant portion of sleep-disordered breathing is associated with ApoE epsilon4 in the general population. 4 key findings →
Design: cohort study Evidence: moderate
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Using parametric methods, no evidence for linkage to the region spanned by the chromosome 12 markers could be detected if familial AD is assumed to arise from the same genetic locus in all 53 families. 2 key findings →
Design: cohort study Participants: 173 Evidence: moderate
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This preliminary report suggests that CETP V405 valine homozygosity is associated with slower memory decline and lower incident dementia and AD risk. 5 key findings →
Design: cohort study Participants: 523 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
However, in this study, the additional risk of dementia conferred by being a first-degree relative, by being female, or by the probability of having an APOE epsilon4 allele appeared similar in African American and white families. 1 key finding →
Participants: 17 Evidence: low
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This study suggests that vitamin E from food, but not other antioxidants, may be associated with a reduced risk of AD. 4 key findings →
Evidence: low
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Fifteen chromosomal regions warranted initial follow-up. 4 key findings →
Participants: 280 Evidence: low
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Among the 30 boxers, 11 were found to be normal (CBI score=0), 12 showed mild deficits (CBI score=1-2), 4 were moderately impaired (CBI score=3-4), and 3 showed signs of severe impairment (CBI score > 4). 3 key findings →
Evidence: low
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Alzheimer disease (AD), the most common cause of dementia in the elderly, exists in both familial and sporadic forms. 3 key findings →
Evidence: low
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Except for autosomal dominant early-onset families, genetic testing in asymptomatic individuals is unwarranted. 5 key findings →
Participants: 20 Evidence: low
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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 →