27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Late-onset Alzheimer's disease (AD) has a significant genetic and immunological component, but the molecular mechanisms through which genetic and immunity-related risk factors and their interplay contribute to AD pathogenesis are unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Black/African American (AA) individuals have a higher risk of Alzheimer's disease (AD) than White non-Hispanic persons of European ancestry (EUR) for reasons that may include economic disparities, cardiovascular health, quality of education, and biases in the methods used to diagnose AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Four out of 10 TREM2 mutant variants have been identified in the analyzed groups, namely rs75932628 C > T (R47H), rs142232675 C > T (D87N), rs143332484 C > T (R62H), and rs2234253 G > T (T96K). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) can be either sporadic or familial, and familial forms of AD accounts for only 5% of the cases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common senile neurodegenerative disease characterized by progressive cognitive dysfunction, psychological and behavioral abnormalities, and impaired ability of activities of daily living. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In a family with autopsy-confirmed Alzheimer disease, the authors found a mutation in the presenilin 2 (PS2) gene (PSEN2) that predicts a methionine-to-isoleucine change at PS2 residue 239 (M239I), at which a change to valine was known in another family. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The mean AAO was 46.9 years (median 45 years; range 33 to 60 years). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified five novel variants in the presenilin1 (PSEN1) gene from Brazilian and Mexican families. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Over 200 rare and fully penetrant pathogenic mutations in amyloid precursor protein (APP), presenilin 1 and 2 (PSEN1 and PSEN2) cause a subset of early-onset familial Alzheimer's disease (EO-FAD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The three female patients had an age of onset of symptoms of 38-51 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It enables robust identification of signaling pathways enriched in disease susceptibility loci. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
42 common genes were identified between OSA and dementia which were primarily linked to the G-coupled protein receptor (GPCR) and olfactory pathways. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Differentially methylated positions (DMPs) between persons with and without late-onset Alzheimer's disease (LOAD) were observed at 477 of 769,190 loci in a plurality of genes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Volga German kindreds are a group of seven related families with autosomal dominant early-onset Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
As the discovery of the Alzheimer's disease (AD) genes, APP, PSEN1, and PSEN2, in families with autosomal dominant early-onset AD (EOAD), gene discovery in familial EOAD came more or less to a standstill. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Metabolomic profiling and the integration of whole-genome genetic association data has proven to be a powerful tool to comprehensively explore gene regulatory networks and to investigate the effects of genetic variation at the molecular level. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration with TAR DNA-binding protein 43 inclusions (FTLD-TDP) is the most common pathology associated with frontotemporal dementia (FTD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the search for new genes in Alzheimer's disease, classic linkage-based and candidate-gene-based association studies have been supplanted by exome sequencing, genome-wide sequencing (for mendelian forms of Alzheimer's disease), and genome-wide association studies (for non-mendelian forms). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
By analyzing late-onset Alzheimer's disease (LOAD) in a genome-wide association study (313,504 SNPs, three series, 844 cases and 1,255 controls) and evaluating the 25 SNPs with the most significant allelic association in four additional series (1,547 cases and 1,209 controls), we identified a SNP (rs5984894) on Xq21.3 in PCDH11X that is strongly associated with LOAD in individuals of European descent from the United States. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Common diseases such as endometriosis (ED), Alzheimer's disease (AD) and multiple sclerosis (MS) account for a significant proportion of the health care burden in many countries. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Studies of long-lived individuals have revealed few genetic mechanisms for protection against age-associated disease. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The immune response, regulation of endocytosis, cholesterol transport, and protein ubiquitination represent prime targets for AD therapeutics. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A fundamental challenge in human health is the identification of disease-causing genes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
While major inroads have been made in identifying the genetic causes of rare Mendelian disorders, little progress has been made in the discovery of common gene variations that predispose to complex diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have led to a rapid increase in available data on common genetic variants and phenotypes and numerous discoveries of new loci associated with susceptibility to common complex diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
9 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 9. The same 9 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 →