27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Strikingly gene-expression, network-based analysis and cell type deconvolution approaches revealed a consistent immune signature in the brain and blood of female AD patients that was absent in males. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The chromosome 9p21 amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) locus contains one of the last major unidentified autosomal-dominant genes underlying these common neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglia play a pivotal role in the maintenance of brain homeostasis but lose homeostatic function during neurodegenerative disorders. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) is a potential and novel biomarker of neuroinflammation implicated in the onset and progression of Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis Participants: 82 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
TREM2 (triggering receptor expressed on myeloid cells 2) gene variants were reported to increase the risk of Alzheimer's disease (AD) and even other neurodegenerative diseases (frontotemporal dementia (FTD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS)), but so far, no definite conclusion has been drawn. 4 key findings →
Design: systematic review Participants: 39 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Recent GWAS studies focused on uncovering novel genetic loci related to AD have revealed associations with variants near CLU, CR1, PICALM and BIN1. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) is a common, fatal motor neuron disorder with no effective treatment. 4 key findings →
Participants: 111 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among 3414 included individuals, the mean (SD) age was 68.8 (6.0) years and 2116 (62%) were female. 5 key findings →
Design: cohort study Participants: 1,184 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
While sex differences were not apparent at asymptomatic stages, females showed more rapid declines across all outcomes in symptomatic stages compared to males. 5 key findings →
Design: longitudinal study Participants: 337 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Common variants within TMEM106B are associated with risk for frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP). 4 key findings →
Design: cohort study Participants: 518 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is a progressive neurodegenerative disorder with no cure, making preventive strategies crucial. 5 key findings →
Design: cohort study Participants: 1,500 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Obesity and Area Deprivation Index, a measure of socioeconomic status, were significantly associated with elevated AD risk within the hypertensive cohort. 4 key findings →
Design: retrospective cohort Participants: 1,862 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The apolipoprotein E type 4 allele (APOE-epsilon 4) is genetically associated with the common late onset familial and sporadic forms of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
To avoid the problems that heterogeneity poses for genetic analysis, the researchers examined the cosegregation of Alzheimer's disease and markers along the long arm of chromosome 21 in a single family. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
A summary measure of γ-secretase activity (γ-secretase composite [GSC]) was calculated for each variant and compared with clinical history-derived AAO using correlation analyses. 3 key findings →
Design: cross-sectional Participants: 190 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The UK Biobank project is a prospective cohort study with deep genetic and phenotypic data collected on approximately 500,000 individuals from across the United Kingdom, aged between 40 and 69 at recruitment.
Full summary, score breakdown and related studies → Original source Free full text
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
E280A carriers had higher p-tau231 levels than non-carriers (9.0 ± 7.4 vs. 5.2 ± 3.4 pg/mL, P < 0.001). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Unlike familial Alzheimer's disease, we have been unable to accurately predict symptom onset in presymptomatic familial frontotemporal dementia (f-FTD) mutation carriers, which is a major hurdle to designing disease prevention trials. 1 key finding →
Design: longitudinal study 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
Compared to non-carriers, APOE ε4 carriers had lower Aβ42/Aβ40 and greater longitudinal increases in p-tau181 and GFAP; in contrast, the AD-PRS (excluding the APOE region) was associated with greater declines in Aβ42/Aβ40 among APOE ε4 non-carriers. 4 key findings →
Design: longitudinal study 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
Nineteen participants developed AD after a median of 60 months (interquartile range 30). 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
10 of the 3,549 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 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 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 →