27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
A total of 1,261 participants from a Chinese community cohort were included and we identified 1 gene, PTPRT, for HV, with the top significant SNPs by whole genome-wide association study (GWAS). rs6030076 (p = 5.48 × 10-8, β = -0.092, SE 0.017) from WES and rs6030088 (p = 8.24 × 10-9, β = -105.22, SE 18.09) from SNP array data were both located in this gene. 5 key findings →
Participants: 1,261 Evidence: moderate
Full summary, score breakdown and related studies → Original source
TREM2 variant carriers (64 ± 7 years, 54% female) did not show distinct clinical measures of AD at presentation compared to AD patients not carrying a TREM2 variant (64 ± 7 years, 52% female). 5 key findings →
Participants: 123 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Epidemiologic studies have reported that cancer survivors have a relatively low risk of developing dementia, but the mechanisms underlying that inverse relationship are mostly unknown. 4 key findings →
Participants: 8,121 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The TMEM106B risk variant was significantly enriched in AD cases with transactive response DNA-binding protein 43 kDa (TDP-43) pathology - associating with increased odds of developing AD TDP-43 subtype α - but failed to associate with Lewy body or vascular pathology. 3 key findings →
Participants: 2,604 Evidence: low
Full summary, score breakdown and related studies → Original source
Multiple MTHFR coding variants were identified in this small Indonesian VaD cohort. 2 key findings →
Design: cross-sectional Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study provides the first molecular characterization of MAPT gene variants in Indonesian patients with vascular dementia. 2 key findings →
Design: cross-sectional Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
The novel respiratory disease COVID-19 produces varying symptoms, with fever, cough, and shortness of breath being common. 3 key findings →
Participants: 16,749 Evidence: low
Full summary, score breakdown and related studies → Original source
UK Biobank is a major prospective epidemiological study, including multimodal brain imaging, genetics and ongoing health outcomes. 1 key finding →
Participants: 8,428 Evidence: low
Full summary, score breakdown and related studies → Original source
People's differences in cognitive functions are partly heritable and are associated with important life outcomes. 5 key findings →
Participants: 36 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We retrospectively assessed the diagnostic accuracy of whole genome sequencing to detect the most common repeat expansion loci associated with neurological outcomes (AR, ATN1, ATXN1, ATXN2, ATXN3, ATXN7, C9orf72, CACNA1A, DMPK, FMR1, FXN, HTT, and TBP) using samples obtained within the National Health Service in England from patients who were suspected of having neurological disorders; previous PCR test results were used as the reference standard. 4 key findings →
Participants: 3,000 Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified >80 Alzheimer's disease and related dementias (ADRD)-associated genetic loci. 3 key findings →
Participants: 7,804 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia and a growing public health burden in the United States. 5 key findings →
Participants: 1,515 Evidence: low
Full summary, score breakdown and related studies → Original source
Although abnormal accumulation of amyloid in the brain is an early biomarker of Alzheimer's disease (AD), wide variation in cognitive trajectories during life can be seen in the setting of brain amyloidosis, ranging from maintenance of normal function to progression to dementia. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher GRS predicted mortality (hazard ratio = 1.05; 95% confidence interval: 1.00-1.10, P = .04). 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Arousal affects cognition, emotion, and behavior and has been implicated in the etiology of psychiatric disorders. 5 key findings →
Participants: 1,877 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified associations in EAs with variants in 12 novel loci. 3 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In order to assess the frequency of mutations in the known Alzheimer's disease causative genes in Turkish dementia patients we screened amyloid precursor protein (APP), PSEN1 and PSEN2 for mutations in a cohort of 98 Turkish dementia families. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this analysis, two single nucleotide polymorphisms in a locus on chromosome 9p21.2 were associated with ALS: rs3849942 (p=2·22×10(-6); odds ratio [OR] 1·39, 95% CI 1·21-1·59) and rs2814707 (p=3·32×10(-6); 1·38, 1·20-1·58). 5 key findings →
Participants: 599 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified rs13374761-A in SLAMF1 gene associated with less memory decline (MAF = 0.071, β= 0.0103, p = 4.14×10-8). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified several risk variants for late-onset Alzheimer's disease (LOAD). 3 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The role of the Alzheimer's Disease Neuroimaging Initiative Genetics Core is to facilitate the investigation of genetic influences on disease onset and trajectory as reflected in structural, functional, and molecular imaging changes; fluid biomarkers; and cognitive status. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Numerous genetic susceptibility and protective markers for AD and disease biomarkers have been identified and replicated using ADNI data and have heavily implicated immune, mitochondrial, cell cycle/fate, and other biological processes. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
SPON1 has not been previously associated with AD risk, but is plausibly related because the gene product binds to the amyloid precursor protein and inhibits its cleavage by β-secretase. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Dominantly Inherited Alzheimer Network (DIAN) is an international registry of individuals at risk for developing autosomal dominant Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The PRS using 131 SNPs had an effect independent of APOE. 5 key findings →
Participants: 565 Evidence: moderate
Full summary, score breakdown and related studies → Original source
10 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 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 27,380 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 →