29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Meta-analysed IVW MR findings suggested that higher GrimAge acceleration increased the risk of colorectal cancer (OR = 1.12 per year increase in GrimAge acceleration, 95% CI 1.04-1.20, p = 0.002). 4 key findings →
Design: meta-analysis Participants: 34,710 Evidence: high
Full summary, score breakdown and related studies → Original source
General cognitive function is substantially heritable across the human life course from adolescence to old age. 5 key findings →
Design: meta-analysis Participants: 53,949 Evidence: high
Full summary, score breakdown and related studies → Original source
Mutations in the gene coding for Sequestosome 1 (SQSTM1) have been genetically associated with amyotrophic lateral sclerosis (ALS) and Paget disease of bone. 5 key findings →
Design: meta-analysis Participants: 3,899 Evidence: high
Full summary, score breakdown and related studies → Original source
Few data are available concerning the role of risk markers for Alzheimer's disease (AD) in progression to AD dementia among subjects with mild cognitive impairment (MCI). 1 key finding →
Design: meta-analysis Participants: 853 Evidence: high
Full summary, score breakdown and related studies → Original source
Among persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment. 4 key findings →
Design: meta-analysis Participants: 2,914 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We identified four plasma protein level PGSs that were significantly associated (FDR-adjusted p < 0.05) with LOAD in a meta-analysis of the discovery and replication cohorts: CX3CL1, hepatocyte growth factor (HGF), TIE2, and matrix metalloproteinase-3 (MMP-3). 4 key findings →
Design: meta-analysis Participants: 17,747 Evidence: high
Full summary, score breakdown and related studies → Original source
Deposition of amyloid plaques in the brain is one of the two main pathological hallmarks of Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis Participants: 1,000 Evidence: high
Full summary, score breakdown and related studies → Original source
Epigenome-wide association studies of Alzheimer's disease have highlighted neuropathology-associated DNA methylation differences, although existing studies have been limited in sample size and utilized different brain regions. 3 key findings →
Design: meta-analysis Participants: 1,453 Evidence: high
Full summary, score breakdown and related studies → Original source
Mass spectrometry-based proteomics empowers deep profiling of proteome and protein posttranslational modifications (PTMs) in Alzheimer's disease (AD). 5 key findings →
Design: meta-analysis Participants: 12,017 Evidence: high
Full summary, score breakdown and related studies → Original source
Consistent with the concept of the gut-brain phenomenon, observational studies suggest a relationship between Alzheimer's disease (AD) and gastrointestinal tract (GIT) disorders; however, their underlying mechanisms remain unclear. 3 key findings →
Design: meta-analysis Participants: 34,652 Evidence: high
Full summary, score breakdown and related studies → Original source
Progressive loss of neurons in a specific brain area is one of the manifestations of Alzheimer's disease (AD). 2 key findings →
Design: meta-analysis Participants: 33,992 Evidence: high
Full summary, score breakdown and related studies → Original source
Among 68 756 unique individuals, analyses included 21 852 East Asian (demographic data not available), 5738 Hispanic (68.2% female; mean [SD] age, 75.4 [8.8] years), 7145 non-Hispanic Black (hereafter referred to as Black) (70.8% female; mean [SD] age, 78.4 [8.2] years), and 34 021 non-Hispanic White (hereafter referred to as White) (59.3% female; mean [SD] age, 77.0 [9.1] years) individuals. 5 key findings →
Design: case-control Participants: 68,756 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The Alzheimer Disease Genetics Consortium (ADGC) performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1) and two replication stages (stages 2 and 3). 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common multifactorial neurodegenerative disease among elderly people. 2 key findings →
Design: meta-analysis Participants: 140 Evidence: high
Full summary, score breakdown and related studies → Original source
Autopsy measures of Alzheimer's disease neuropathology have been leveraged as endophenotypes in previous genome-wide association studies (GWAS). 2 key findings →
Design: meta-analysis Participants: 2,701 Evidence: high
Full summary, score breakdown and related studies → Original source
We identified and validated five novel gene associations in cortical brain tissue ( PRKAG1 , C3orf62 , LYSMD4 , ZNF439 , SLC11A2 ) and six genes proximal to known AD-related GWAS loci (Blood: MYBPC3 ; Brain: MTCH2 , CYB561 , MADD , PSMA5 , ANXA11 ). 3 key findings →
Design: meta-analysis Participants: 2,683 Evidence: high
Full summary, score breakdown and related studies → Original source
This 2026 update is an even larger follow-up to the 2022 Bellenguez GWAS, combining data from nearly 1 million people. 5 key findings →
Design: meta-analysis Participants: 978,514 Evidence: high
Full summary, score breakdown and related studies → Original source
As the first 1-year, multinational, double-blinded, placebo-controlled study of a cholinesterase inhibitor in AD, these data support donepezil as a well tolerated and effective long-term treatment for patients with AD, with benefits over placebo on global assessment, cognition, and ADL. 3 key findings →
Participants: 286 Evidence: high
Full summary, score breakdown and related studies → Original source
Intelligence is highly heritable 1 and a major determinant of human health and well-being 2 . 2 key findings →
Design: meta-analysis Participants: 269,867 Evidence: high
Full summary, score breakdown and related studies → Original source
Collecting cases for case-control genetic association studies can be time-consuming and expensive. 1 key finding →
Design: meta-analysis Participants: 116,196 Evidence: high
Full summary, score breakdown and related studies → Original source
Due to the small number of studies and heterogeneity in study design and outcomes, the association between DNA methylation age and age-related disease and longevity is inconclusive. 3 key findings →
Design: systematic review Participants: 41,607 Evidence: high
Full summary, score breakdown and related studies → Original source
The genetic basis of Alzheimer's disease (AD) is complex and heterogeneous. 4 key findings →
Design: meta-analysis Participants: 3,500 Evidence: high
Full summary, score breakdown and related studies → Original source
We present robust evidence for elevated DNA methylation associated with Alzheimer's disease neuropathology spanning the HOXA gene cluster on chromosome 7. 4 key findings →
Design: meta-analysis Participants: 117 Evidence: high
Full summary, score breakdown and related studies → Original source
For ACD, novel loci identified were associated with energy transport (SEMA4D), neuronal excitability (ANO3), amyloid deposition in the brain (RBFOX1), and magnetic resonance imaging markers of small vessel disease (SVD; HBEGF). 5 key findings →
Participants: 800,597 Evidence: low
Full summary, score breakdown and related studies → Original source
Iron deposition in the brain is a prominent feature of Alzheimer's disease (AD). 3 key findings →
Design: meta-analysis Participants: 24,000 Evidence: high
Full summary, score breakdown and related studies → Original source
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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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 (3.5% 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 →