27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
General cognitive function is substantially heritable across the human life course from adolescence to old age. 5 key findings →
Design: meta-analysis Participants: 53,949 Evidence: high
Full summary, score breakdown and related studies → Original source
We identified four plasma protein level PGSs that were significantly associated (FDR-adjusted p < 0.05) with LOAD in a meta-analysis of the discovery and replication cohorts: CX3CL1, hepatocyte growth factor (HGF), TIE2, and matrix metalloproteinase-3 (MMP-3). 4 key findings →
Design: meta-analysis Participants: 17,747 Evidence: high
Full summary, score breakdown and related studies → Original source
The APOE4 allele, but not AD-GRS, was associated with baseline lower hippocampus volume (β = -0.27, p = 0.001), greater amyloid deposition (β = 0.48, p = 0.001), 2-year decline in hippocampus (β = -0.27, p = 0.01), total gray matter volume (β = -0.25, p = 0.01), and cortical thickness (β = -0.28, p = 0.003). 5 key findings →
Participants: 126 Evidence: high
Full summary, score breakdown and related studies → Original source
Significant study-site, specimen type, and batch effects were observed. 5 key findings →
Design: randomized controlled trial Participants: 604 Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common multifactorial neurodegenerative disease among elderly people. 2 key findings →
Design: meta-analysis Participants: 140 Evidence: high
Full summary, score breakdown and related studies → Original source
Autopsy measures of Alzheimer's disease neuropathology have been leveraged as endophenotypes in previous genome-wide association studies (GWAS). 2 key findings →
Design: meta-analysis Participants: 2,701 Evidence: high
Full summary, score breakdown and related studies → Original source
We identified and validated five novel gene associations in cortical brain tissue ( PRKAG1 , C3orf62 , LYSMD4 , ZNF439 , SLC11A2 ) and six genes proximal to known AD-related GWAS loci (Blood: MYBPC3 ; Brain: MTCH2 , CYB561 , MADD , PSMA5 , ANXA11 ). 3 key findings →
Design: meta-analysis Participants: 2,683 Evidence: high
Full summary, score breakdown and related studies → Original source
Intelligence is highly heritable 1 and a major determinant of human health and well-being 2 . 2 key findings →
Design: meta-analysis Participants: 269,867 Evidence: high
Full summary, score breakdown and related studies → Original source
Collecting cases for case-control genetic association studies can be time-consuming and expensive. 1 key finding →
Design: meta-analysis Participants: 116,196 Evidence: high
Full summary, score breakdown and related studies → Original source
For ACD, novel loci identified were associated with energy transport (SEMA4D), neuronal excitability (ANO3), amyloid deposition in the brain (RBFOX1), and magnetic resonance imaging markers of small vessel disease (SVD; HBEGF). 5 key findings →
Participants: 800,597 Evidence: low
Full summary, score breakdown and related studies → Original source
Iron deposition in the brain is a prominent feature of Alzheimer's disease (AD). 3 key findings →
Design: meta-analysis Participants: 24,000 Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common neurodegenerative disease. 2 key findings →
Design: meta-analysis Participants: 74,046 Evidence: high
Full summary, score breakdown and related studies → Original source
These results provide new insight into the genetic basis of habitual PA, and the genetic links connecting PA with other traits and diseases. 5 key findings →
Design: meta-analysis Participants: 8,556 Evidence: high
Full summary, score breakdown and related studies → Original source
In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. 2 key findings →
Design: meta-analysis Participants: 1,743 Evidence: high
Full summary, score breakdown and related studies → Original source
We developed an endophenotype disease module-based methodology for Alzheimer's disease (AD) drug repurposing and identified sildenafil as a potential disease risk modifier. 2 key findings →
Design: case-control study Evidence: high
Full summary, score breakdown and related studies → Original source
The aims of this study were to identify candidate single nucleotide polymorphisms (SNPs) and mechanisms of Alzheimer's disease (AD) and to generate SNP to gene to pathway hypotheses. 5 key findings →
Design: meta-analysis Participants: 370,542 Evidence: high
Full summary, score breakdown and related studies → Original source
GWAS of Alzheimer's disease have been predominantly based on European ancestry cohorts with clinically diagnosed patients. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
This situation presents difficulties for experimental studies, drug development, and other future research. 5 key findings →
Design: meta-analysis Participants: 94 Evidence: high
Full summary, score breakdown and related studies → Original source
The use of quantitative endophenotypes in genetic studies may provide greater power, allowing for the use of powerful statistical methods and a biological model for the effects of the disease-associated genetic variation. 1 key finding →
Design: meta-analysis Participants: 313 Evidence: high
Full summary, score breakdown and related studies → Original source
Lewy body dementia (LBD) is the second most prevalent dementia, however most genetic risk remains uncharacterized. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Genome-wide association studies have discovered numerous genomic loci associated with Alzheimer's disease (AD); yet the causal genes and variants are incompletely identified. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
The primary genetic risk factor for late onset Alzheimer's disease (LOAD) is the APOE4 allele of Apolipoprotein E (APOE) gene. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Cognitive impairment was observed in 65 patients (42.5%) during a mean follow-up of 37.7 ± 12.4 months. 5 key findings →
Design: cohort study Participants: 153 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) of Alzheimer's disease are predominantly carried out in European ancestry individuals despite the known variation in genetic architecture and disease prevalence across global populations. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Previously reported pathogenic variants in the six genes were identified in 1.35% of EOAD (3/223) and 6.58% of EOnonAD (5/76). 5 key findings →
Design: longitudinal study Participants: 299 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 →