27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Age-related cognitive decline is likely promoted by accumulated brain injury due to chronic conditions of aging, including neurodegenerative and vascular disease. 4 key findings →
Participants: 749 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) is a complex polygenic neurodegenerative disorder. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nine PSEN2 rare variants were found, including two reported (M239T, R62C) and seven novel variants (N141S, I368F, L396I, G117X, I146T, S147N, H220Y). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Functional phenotypes (e.g., subcortical surface representation), which commonly arise in imaging genetic studies, have been used to detect putative genes for complexly inherited neuropsychiatric and neurodegenerative disorders. 2 key findings →
Participants: 708 Evidence: low
Full summary, score breakdown and related studies → Original source
Preclinical models of Alzheimer's disease (AD) suggest APOE modulates brain function in structures vulnerable to AD pathophysiology. 5 key findings →
Participants: 608 Evidence: low
Full summary, score breakdown and related studies → Original source
Gene-based PRS identified 389 genes with 164 of them not previously reported as AD-associated. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has multiple clinically and pathologically defined subtypes where the underlying causes of such heterogeneity are not well established. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified a PSEN1 variant (p.Thr291Pro) in an individual presenting with pure SP at 30 years of age. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations of 3 causative genes, namely presenilin 1 (PSEN1), presenilin 2 (PSEN2), and amyloid precursor protein (APP), have been identified as the major causes of early-onset familial Alzheimer's disease (EOFAD). 5 key findings →
Participants: 32 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although Alzheimer's disease (AD) is a central nervous system disease and type 2 diabetes MELLITUS (T2DM) is a metabolic disorder, an increasing number of genetic epidemiological studies show clear link between AD and T2DM. 5 key findings →
Participants: 448 Evidence: low
Full summary, score breakdown and related studies → Original source
Potential pharmacogenetic biomarkers for AD have been identified; however, it is still necessary to conduct further research into other populations and to identify new biomarkers. 2 key findings →
Participants: 33 Evidence: low
Full summary, score breakdown and related studies → Original source
We identified chemicals enriched for dementia pathways, suggesting broad classes of chemicals contribute to dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a genetically complex and heterogeneous disorder. 2 key findings →
Participants: 2,700 Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified many risk loci for Alzheimer's disease (AD) 1,2 , but how these loci confer AD risk is unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Polygenic Risk Scores (PRS) for AD offer unique possibilities for reliable identification of individuals at high and low risk of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Within this region, we defined a 42-SNP haplotype that was associated with significantly increased risk of ALS (p=7·47×10(-33) when people with familial ALS were compared with controls, odds ratio 21·0, 95% CI 11·2-39·1) and which overlapped with an association locus recently reported for frontotemporal dementia. 1 key finding →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
We confirm that variation in/near APOE/TOMM40 (P = 6 × 10(-14)) alters PCA risk, but with smaller effect than for typical AD (PCA: odds ratio [OR] = 2.03, typical AD: OR = 2.83, P = .0007). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Large studies (e.g. UK Biobank) are increasingly used for GWAS and Mendelian randomization (MR) studies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In a multivariate analysis, associations of MS4A6A (rs610932; odds ratio = 0.632, Bonferroni corrected P = .019) and CD33 (rs3865444; odds ratio = 1.492, Bonferroni corrected P = .017) with LOAD were replicated successfully. 5 key findings →
Participants: 1,224 Evidence: low
Full summary, score breakdown and related studies → Original source
Our analysis of common SNVs and indels confirmed known genetic loci at MAPT, MOBP, STX6, SLCO1A2, DUSP10, and SP1, and further uncovered novel signals in APOE, FCHO1/MAP1S, KIF13A, TRIM24, TNXB, and ELOVL1. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The data processing pipelines, research-ready imputed genetic data, and PRS scores are now available on the DPUK platform and can be accessed upon request though the DPUK application process. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We calculated a PRS for LOY in 5131 men aged 70 years and older. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia, a collective term for neurodegenerative disorders marked by cognitive decline, affects millions worldwide, and is expected to rise significantly in prevalence. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Seventeen variants were significantly associated with AD within five genomic regions implicating the genes OARD1/NFYA/TREML1, JAZF1, FERMT2, and SLC24A4. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Some viruses, such as varicella zoster virus, are associated with severe dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
8 of the 346 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 8. The same 8 appear here every time.
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 →