28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our data reveal an association of APOE ε3/3- TOMM40 '523 haplotypes with cognitive decline in community-based older persons such that the S/S poly-T genotype is related to faster cognitive decline, primarily in the domains of episodic and semantic memory. 1 key finding →
Design: cohort study Evidence: moderate
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The single nucleotide polymorphism rs1080985 in the CYP2D6 gene may influence the clinical efficacy of donepezil in patients with mild to moderate Alzheimer disease (AD). 3 key findings →
Design: cohort study Participants: 115 Evidence: moderate
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A slower rate of hippocampal atrophy in normal APOE2 carriers is consistent with the lower risk of Alzheimer disease in these individuals. 5 key findings →
Design: cohort study Participants: 72 Evidence: moderate
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Women show better verbal memory than men in aMCI despite similar levels of brain hypometabolism. 4 key findings →
Design: cross-sectional Participants: 672 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOE epsilon 4 may influence rate of cognitive decline most significantly in the earliest stages of Alzheimer disease. 3 key findings →
Design: cohort study Evidence: moderate
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This advantage may represent a sex-specific form of cognitive reserve delaying verbal memory decline until more advanced disease stages. 1 key finding →
Design: cross-sectional Participants: 379 Evidence: low
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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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Alzheimer disease pathologic changes are common in DLB and are associated with the clinical phenotype. β-Amyloid is associated with cognitive impairment, and tau pathology is associated with lower frequency of clinical features of DLB. 5 key findings →
Participants: 417 Evidence: moderate
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The results of this study indicate that the DMN abnormalities observed in patients with AD represent an accelerated aging pattern of connectivity compared with matched controls. 3 key findings →
Participants: 28 Evidence: moderate
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In addition to known candidate genes, APOE, TOMM40, and one hypothetical gene LOC100129500 partially overlapping APOE; one novel gene, EPC2, and several other interesting genes were associated with CSF biomarkers that are related to AD. 3 key findings →
Participants: 374 Evidence: moderate
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Arterial stiffness, measured by PWV, is an emerging risk factor for dementia through its repeated relationships with cognition, cSVD, and Aβ deposition. 4 key findings →
Design: cross-sectional Evidence: low
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A total of 1,261 participants from a Chinese community cohort were included and we identified 1 gene, PTPRT, for HV, with the top significant SNPs by whole genome-wide association study (GWAS). rs6030076 (p = 5.48 × 10-8, β = -0.092, SE 0.017) from WES and rs6030088 (p = 8.24 × 10-9, β = -105.22, SE 18.09) from SNP array data were both located in this gene. 5 key findings →
Participants: 1,261 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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Elderly patients with diabetes develop more extensive vascular pathology, which alone or together with AD-type pathology (particularly in APOE ε4 carriers) results in increased dementia risk. 2 key findings →
Participants: 553 Evidence: low
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Four plasma analytes were consistently associated with the diagnosis of very mild dementia/MCI/AD in 3 independent clinical cohorts. 3 key findings →
Participants: 566 Evidence: moderate
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Adherence to the Mediterranean diet (MeDi) may affect not only risk for Alzheimer disease (AD) but also subsequent disease course: Higher adherence to the MeDi is associated with lower mortality in AD. 5 key findings →
Participants: 192 Evidence: low
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The MIND and Mediterranean diets are associated with less postmortem AD pathology, primarily β-amyloid load. 5 key findings →
Participants: 581 Evidence: low
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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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Within APOE ε4 carriers, sex differences in CSF p-Tau are more evident in early disease stages, whereas for APOE ε4 noncarriers, sex differences are more evident in advanced disease stages. 3 key findings →
Participants: 1,801 Evidence: low
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Even in a highly selected lifespan sample of adults, Aβ deposition is apparent in some adults and is influenced by APOE status. 5 key findings →
Participants: 137 Evidence: low
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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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As potential harbingers of future cognitive decline, physicians should query and monitor SMCs from their older patients. 1 key finding →
Participants: 531 Evidence: moderate
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The data do not support an association between serum total cholesterol or high density lipoprotein in late life and subsequent risk of dementia or Alzheimer disease (AD). 5 key findings →
Design: cohort study Evidence: moderate
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The APOE-4 allele increases risk and decreases age at onset of PD, an association that may not be dependent upon cognitive impairment. 3 key findings →
Design: case-control study Evidence: moderate
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AD biomarkers are useful to predict AD-type dementia in subjects with aMCI and naMCI. 4 key findings →
Participants: 231 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 →