Dementia is a leading cause of death in many countries. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Dementia is a leading cause of death in many countries. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
In addition to apolipoprotein E (APOE), recent large genome-wide association studies (GWASs) have identified nine other genes/loci (CR1, BIN1, CLU, PICALM, MS4A4/MS4A6E, CD2AP, CD33, EPHA1 and ABCA7) for late-onset Alzheimer's disease (LOAD). 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
We undertook a genome-wide association study (GWAS) of parental longevity in European descent UK Biobank participants. 4 key findings →
Design: longitudinal study Participants: 1,181 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We developed a new statistical framework to find genetic variants associated with extreme longevity. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
We found that common variation at the CR1 locus has a broad impact on cognition and that this effect is largely mediated by an individual's amyloid plaque burden. 4 key findings →
Design: cohort study Participants: 1,666 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) is a multi-system disease characterized primarily by progressive muscle weakness. 2 key findings →
Design: longitudinal study Participants: 327 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Most people's cognitive abilities decline with age, with significant and partly genetically driven, individual differences in rate of change. 3 key findings →
Design: longitudinal study Participants: 1,087 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Familial Alzheimer's disease (FAD), despite representing a rare condition, is attracting a growing interest in the scientific community. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Variants in GBA, encoding the enzyme glucocerebrosidase, are associated with Lewy body diseases such as Parkinson's disease and Lewy body dementia. 5 key findings →
Design: case-control study Participants: 165 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genetic variation in sulfonylurea targets was associated with a lower risk of AD, and future studies are warranted to clarify the underlying mechanistic pathways between sulfonylureas and AD. 5 key findings →
Participants: 326,885 Evidence: low
Full summary, score breakdown and related studies → Original source
PheMap significantly streamlines the process of extracting research-quality phenotype information from EHRs, with comparable or better performance to current phenotyping approaches. 3 key findings →
Design: case-control study Participants: 821 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among 463,447 TPMI participants, 4381 PD patients and 43,810 controls were analysed. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent studies have found an association between a variant in triggering receptor expressed on myeloid cells 2 (TREM2) (rs75932628-T) and both Alzheimer's disease (AD) and cognitive function in individuals aged 80-100 years. 2 key findings →
Design: longitudinal study Participants: 1,148 Evidence: moderate
Full summary, score breakdown and related studies → Original source
MTUS2 encodes a microtubule associated protein implicated in the development and function of the nervous system, making it a plausible candidate to investigate LOAD biology. 4 key findings →
Participants: 14,260 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genome-wide significant loci were identified for all biomarkers, including DACT1-DAAM1 (pTau217), KCNJ3 (pTau181), KLHDC4 (NfL), SLC10A7 (GFAP), and PPP4R2 (composite score). 4 key findings →
Participants: 1,972 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma levels of glial fibrillary acidic protein (GFAP) and neurofilament light (NEFL) are key dementia biomarkers. 3 key findings →
Participants: 50,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Approximately 40% of dementia cases could be prevented or delayed by modifiable risk factors related to lifestyle and environment. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Rich data from large biobanks, coupled with increasingly accessible association statistics from genome-wide association studies (GWAS), provide great opportunities to dissect the complex relationships among human traits and diseases. 5 key findings →
Participants: 61,212 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder and the most common form of dementia in the elderly. 2 key findings →
Design: case-control study Participants: 931 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Using hippocampal atrophy as a quantitative phenotype in a genome-wide scan, we have identified candidate risk genes for sporadic Alzheimer's disease that merit further investigation. 1 key finding →
Design: case-control study Participants: 381 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Polygenic Risk Score significantly predicted the risk associated with age at AD onset when SNPs were preselected for association to AD at P ≤ 0.001. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The established association of APOE*4 carriers with AD was confirmed in this community-based sample of older subjects (odds ratio (OR) = 2.22; p = 9.36E-14) and was stronger in females (OR = 2.72; p = 1.74E-10) than in males (OR = 1.88; p = 2.43E-05). 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tau and amyloid beta (Aβ) proteins accumulate along neuronal circuits in Alzheimer's disease. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Six patients with AD with GSN P3fs and K346fs mutations (0.50%, 6/1192) were identified, who were diagnosed with AD but not FAF. 5 key findings →
Participants: 1,192 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The PRS for AD was significantly higher in APOE ε4 homozygote AD cases compared to older cognitively healthy APOE ε4/ε4 controls (odds ratio [OR] 8.39; confidence interval [CI] 2.0-35.2; P = .003). 4 key findings →
Participants: 213 Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 359 studies in this tag that have a study page, 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 10. The same 10 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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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 →