27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The genetics dataset yielded two subtypes of AD characterized mainly by the presence/absence of the apolipoprotein E (APOE) ε4 genotype, but also involving differential presence of risk alleles of CD2AP, SPON1 and LOC39095 SNPs that were associated with differences in the respective patterns of brain atrophy, especially in the precuneus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies have associated clusterin (CLU) variants with Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our data indicated that 18p11.32 (rs1992269, P = 9.77 × 10(-7)), CNTNAP2 (rs802571, P = 1.26 × 10(-6)), and 12q24.23 (rs11613092, P = 6.85 × 10(-6)) were suggestive loci for susceptibility to LOAD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) are a powerful tool for understanding the genetic underpinnings of human disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Large case/control genome-wide association studies (GWAS) often include groups of related individuals with known relationships. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Important methodological advancements in rare variant association testing have been made recently, among them collapsing tests, kernel methods and the variable threshold (VT) technique. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified 1 known pathogenic PSEN1 (p.His163Arg, c.488A>G) mutation and 3 novel PSEN2 mutations in 6 patients. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), the most common form of senile dementia, is a genetically complex disorder. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a clinically heterogeneous neurodegenerative disease with a strong genetic component. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies are identifying novel Alzheimer's disease (AD) risk factors. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The structure of the human brain is highly heritable, and is thought to be influenced by many common genetic variants, many of which are currently unknown. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex disorder with a clear genetic component. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is an age-related progressive neurodegenerative disorder. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have gained considerable momentum over the last couple of years for the identification of novel complex disease genes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
At present, the etiology of Alzheimer's disease (AD) is still unclear, but both genetic and non-genetic factors are thought to take part in the etiopathogenesis of AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, GWAS of complex diseases and traits have focused less on individual susceptibility variants and instead have emphasized the biological pathways and networks revealed by genetic associations. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We performed a systematic, large-scale analysis of human protein complexes comprising gene products implicated in many different categories of human disease to create a phenome-interactome network. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Psychiatric disorders are among the most intractable enigmas in medicine. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease is the most common cause of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this paper, we develop a method based on support vector machines (SVMs) that starting from the protein sequence information can predict whether a new phenotype derived from a nsSNP can be related to a genetic disease in humans. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
To better characterize the genetic architecture underlying Alzheimer's disease (AD) and related dementia (ADRD), we performed a meta-analysis of European ancestry genome-wide association studies in 128,681 cases or proxy cases of ADRD and 849,833 (proxy) controls. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Established AD risk factors, including APOE ε4 dosage and polygenic risk scores, were not associated with disease progression amyloid positive individuals who are actively declining. 5 key findings →
Design: meta-analysis Participants: 222 Evidence: high
Full summary, score breakdown and related studies → Original source
Almost every recent Alzheimer's disease (AD) genome-wide association study (GWAS) has performed meta-analysis to combine studies with clinical diagnosis of AD with studies that use proxy phenotypes based on parental disease history. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
The cross-ancestry Bayesian PRS model demonstrated the highest predictive performance in non-European populations. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The global outbreak of COVID-19, caused by the SARS-CoV-2 virus, has been linked to long-term neurological complications, including an increased risk of Alzheimer's disease (AD) among older adults. 4 key findings →
Evidence: low
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 →