27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The GWAS identified a significant single nucleotide polymorphism (SNP), rs17149074, within the C9orf171 (CFAP77) gene region that showed significant association with changes in CSF t-tau over time. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
Full summary, score breakdown and related studies → Original source
Gaining insight into the downstream consequences of non-coding variants is an essential step towards the identification of therapeutic targets from genome-wide association study (GWAS) findings. 4 key findings →
Participants: 31,684 Evidence: low
Full summary, score breakdown and related studies → Original source
Brain amyloid deposition is thought to be a seminal event in Alzheimer’s disease. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Growing evidence indicates that apolipoprotein E (ApoE) is one of the most important candidate genes for influencing the development of hemodialysis (HD). 3 key findings →
Design: case-control study Participants: 485 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genetic risk for AD does not modify the association between hypertension and dementia. 4 key findings →
Design: cohort Participants: 11,597 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Apolipoprotein E is immunochemically localized to the senile plaques, vascular amyloid, and neurofibrillary tangles of Alzheimer disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The association between the apoE epsilon4 allele and Alzheimer disease does not seem to be mediated by vascular factors. 1 key finding →
Participants: 1,449 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The current conceptualization of Alzheimer disease (AD) is driven by the amyloid hypothesis, in which a deterministic chain of events leads from amyloid deposition and then tau deposition to neurodegeneration and progressive cognitive impairment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Although Aβ did not differ by sex, cognitive decline was greater in females with higher Aβ. 3 key findings →
Participants: 755 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
The presence of epsilon 4 was associated with risk of developing AD on follow-up (relative risk, 1.92; 95% confidence interval, 1.27-2.89). 3 key findings →
Design: cohort study Participants: 624 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Although there were no significant differences among the 3 groups of participants in their clinical ratings, neuropsychological test scores, hippocampal volumes (P = .60), or hippocampal glucose metabolism measurements (P = .12), there were significant group differences in their posterior cingulate glucose metabolism measurements (P = .001). 2 key findings →
Design: cross-sectional Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Targeted sequencing of confirmed GWAS loci revealed an excess burden of deleterious coding mutations in LOAD, with the greatest burden observed in ABCA7 and BIN1. 4 key findings →
Participants: 176 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The impact of APOE4 on brain metabolism and structure is modified by sex. 3 key findings →
Design: cross-sectional Participants: 274 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results suggest that, to optimize observing a treatment effect, clinical trials enrolling cognitively normal individuals should selectively recruit participants with abnormal levels of both amyloid and tau (ie, stage 2) because this group would be expected to show the greatest cognitive decline over time if untreated. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Compared with individuals with the APOEepsilon3/epsilon3, the odds of having AD were significantly increased among those with 1 or more copies of the epsilon4 allele; the odds ratio (OR) for the epsilon3/epsilon4 genotype was 2.6 (95% confidence interval [CI], 1.8-3.7), and the OR for the epsilon4/epsilon4 genotype was 10.5 (95% CI, 5.1-21.8). 3 key findings →
Design: case-control study Participants: 338 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Full summary, score breakdown and related studies → Original source Free full text
Among 4392 participants (mean [SD] age, 68.2 [7.8] years; 2359 [53.7%] women), 723 (16.5%) were APOE ε4 heterozygotes and 33 (0.8%) were APOE ε4 homozygotes. 5 key findings →
Design: cohort study Participants: 4,392 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of 413 477 All of Us participants, 2038 were eligible. 5 key findings →
Design: cohort study Participants: 26 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Disclosure (N = 194) and non-disclosure (N = 180) groups did not differ on IGT-AD (mean disclosure-non-disclosure difference [MD] at 6 weeks: -1.5, p = 0.14; 9 months: -1.2, p = 0.35; 15 months: -2.0, p = 0.07), IES-R (MD at 6 weeks: 0.00, p = 0.98; 9 months: 0.01, p = 0.84; 15 months: 0.03, p = 0.64), or change in secondary outcomes. 4 key findings →
Design: randomized controlled trial Participants: 194 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late-onset, sporadic Alzheimer's disease (AD).
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. 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 27,780 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 →