27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The APOE ϵ4 allele is a strong risk factor across the LBD spectrum and occurs at an increased frequency in pDLB relative to PDD. 4 key findings →
Design: case-control study Participants: 244 Evidence: moderate
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Low frequency coding variants in TREM2 are associated with increased Alzheimer disease (AD) risk, while loss of functions mutations in the gene lead to an autosomal recessive early-onset dementia, named Nasu-Hakola disease (NHD). 5 key findings →
Design: case-control study Participants: 180 Evidence: moderate
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The APOE genotype is an important determinant of the risk of dementia. 1 key finding →
Design: cohort study Participants: 134 Evidence: moderate
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To discover susceptibility genes of late-onset Alzheimer's disease (LOAD), we conducted a 3-stage genome-wide association study (GWAS) using three populations: Japanese from the Japanese Genetic Consortium for Alzheimer Disease (JGSCAD), Koreans, and Caucasians from the Alzheimer Disease Genetic Consortium (ADGC). 1 key finding →
Participants: 1,008 Evidence: low
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We identified 4 novel genetic loci that implicate inflammatory and glial proliferative pathways in the development of WMH in addition to previously proposed ischemic mechanisms. 2 key findings →
Design: meta-analysis Participants: 17 Evidence: high
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Whether novel risk variants of Alzheimer's disease (AD) identified through genome-wide association studies also influence magnetic resonance imaging-based intermediate phenotypes of AD in the general population is unclear. 4 key findings →
Design: meta-analysis Participants: 8,175 Evidence: high
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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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PurposeTelephone disclosure of genetic test results can improve access to services. 4 key findings →
Participants: 257 Evidence: high
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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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This study aimed to evaluate the impact of APOE4 homozygosity on Alzheimer's disease (AD) by examining its clinical, pathological and biomarker changes to see whether APOE4 homozygotes constitute a distinct, genetically determined form of AD. 2 key findings →
Participants: 3,297 Evidence: low
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The eMERGE (electronic MEdical Records and GEnomics) Network is an NHGRI-supported consortium of five institutions to explore the utility of DNA repositories coupled to Electronic Medical Record (EMR) systems for advancing discovery in genome science. eMERGE also includes a special emphasis on the ethical, legal and social issues related to these endeavors. 2 key findings →
Design: meta-analysis Evidence: high
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Vitamin E had no benefit in patients with mild cognitive impairment. 5 key findings →
Participants: 769 Evidence: low
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TREM2 is a transmembrane receptor that is predominantly expressed by microglia in the central nervous system. 4 key findings →
Design: cross-sectional Participants: 1,027 Evidence: moderate
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TREM and TREM-like receptors are a structurally similar protein family encoded by genes clustered on chromosome 6p21.11. 4 key findings →
Design: meta-analysis Evidence: high
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These findings provide evidence for a relationship between all types of alcohol use and increased dementia risk. 5 key findings →
Design: cohort Participants: 559,559 Evidence: moderate
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The large number of participants screened with amyloid positron emission tomography (PET) and standardized assessments provides an unprecedented opportunity to evaluate factors associated with elevated brain amyloid. 5 key findings →
Design: cross-sectional Participants: 4,486 Evidence: low
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The clinical diagnosis of probable AD dementia demonstrated good agreement with biologically defined AD (positive predictive value 85.2%). 3 key findings →
Design: cohort study Participants: 166 Evidence: moderate
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Brain DNA methylation in multiple AD loci is associated with AD pathologies. 5 key findings →
Design: cohort study Participants: 447 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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This study shows that PUTG component scores were significantly associated with diagnostic group and AD biomarkers, a finding that was more pronounced in APOE ε4 carriers. 5 key findings →
Design: longitudinal study Participants: 689 Evidence: moderate
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We identified a new genetic risk association of AD with rare coding CLU variations that is independent of the 5' common association signal identified in the GWA studies. 3 key findings →
Design: meta-analysis Participants: 1,930 Evidence: high
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These samples were graded on an ordinal scale and genotyped for variants associated with synucleinopathies. 2 key findings →
Participants: 213 Evidence: moderate
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Alzheimer's disease (AD), the leading cause of dementia, has an estimated heritability of approximately 70% 1 . 3 key findings →
Participants: 32,558 Evidence: low
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Arterial stiffness was associated with Aβ plaque deposition in the brain, independent of BP and APOE ε4 allele. 5 key findings →
Participants: 91 Evidence: moderate
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Brain iron elevation is implicated in Alzheimer's disease (AD) pathogenesis, but the impact of iron on disease outcomes has not been previously explored in a longitudinal study. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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.
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →