Fine-mapping is commonly used to identify putative causal variants at genome-wide significant loci. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Fine-mapping is commonly used to identify putative causal variants at genome-wide significant loci. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has no cure, but early detection and risk prediction could allow earlier intervention. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Developing Alzheimer's disease (AD) is influenced by multiple genetic variants that are involved in five major AD-pathways. 5 key findings →
Design: longitudinal study Participants: 1,895 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings indicate shared genetic susceptibility to AD and small vessel stroke and highlight potential causal pathways and loci. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Associations are present between environmental risk factors for AD and age acceleration. 1 key finding →
Design: longitudinal study Participants: 5,100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among Caucasian subjects from clinic- or autopsy-based studies, the risk of AD was significantly increased for people with genotypes epsilon2/epsilon4 (OR=2.6, 95% CI=1.6-4.0), epsilon3/epsilon4 (OR=3.2, 95% CI=2.8-3.8), and epsilon4/epsilon4 (OR=14.9, 95% CI= 10.8-20.6); whereas, the ORs were decreased for people with genotypes epsilon2/epsilon2 (OR=0.6, 95% CI=0.2-2.0) and epsilon2/epsilon3 (OR=0.6, 95% CI=0.5-0.8). 2 key findings →
Participants: 5,930 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The presence of an APOE-epsilon4 allele is a determinant of AD risk in whites, but African Americans and Hispanics have an increased frequency of AD regardless of their APOE genotype. 2 key findings →
Design: longitudinal study Participants: 1,079 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dementia was associated with mortality in 70% of older adults with DS. 5 key findings →
Design: longitudinal study Participants: 300 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Over 10 years of close clinical dementia surveillance in this cohort study, loneliness was associated with increased dementia risk; this tripled in adults whose baseline risk would otherwise be relatively low on the basis of age and genetic risk, representing a majority of the US population. 5 key findings →
Design: cohort study Participants: 2,308 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Increased levels of triglycerides at midlife predict brain Aβ and tau pathology 20 years later in cognitively healthy individuals. 5 key findings →
Design: cohort study Participants: 134 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of 4467 participants who underwent 9208 longitudinal cognitive sessions, 2698 (60.4%) were female, and the mean age (SD) was 74.3 (9.2) years; 3213 were cognitively unimpaired, 972 had mild cognitive impairment, and 282 had AD dementia. 2 key findings →
Design: cohort study Participants: 4,467 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Targeted analysis of 20 SNPs that were reported to be associated with ADRD revealed that six were significantly associated with dual-disease outcomes, specifically congestive heart failure and cancer. 4 key findings →
Design: longitudinal study Participants: 1,177 Evidence: moderate
Full summary, score breakdown and related studies → Original source
First, we mapped SVs across 81 AD risk loci and discovered 22 SVs in linkage disequilibrium (LD) with GWAS lead variants and directly associated with the phenotypes tested. 5 key findings →
Design: cohort study Participants: 1,088 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A one standard deviation increase in AD-PGS was associated with an accelerated time to dementia diagnosis by 4.8 months. 5 key findings →
Design: prospective cohort Participants: 7,039 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →