GWAS of Alzheimer's disease have been predominantly based on European ancestry cohorts with clinically diagnosed patients. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
GWAS of Alzheimer's disease have been predominantly based on European ancestry cohorts with clinically diagnosed patients. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Genetic discoveries of Alzheimer's disease are the drivers of our understanding, and together with polygenetic risk stratification can contribute towards planning of feasible and efficient preventive and curative clinical trials. 2 key findings →
Design: case-control study Participants: 409,435 Evidence: moderate
Full summary, score breakdown and related studies → Original source
White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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
Chronological age offers an imperfect estimate of the molecular changes that occur with aging. 4 key findings →
Participants: 4,000 Evidence: low
Full summary, score breakdown and related studies → Original source
Dysregulated microglia activation, leading to neuroinflammation, is crucial in neurodegenerative disease development and progression. 1 key finding →
Participants: 90,716 Evidence: low
Full summary, score breakdown and related studies → Original source
The APOE-ε4/ε4 genotype is the strongest genetic risk factor for sporadic Alzheimer's disease, though the relative risk is diminished in individuals with African ancestry. 2 key findings →
Design: case-control Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Genetic studies of Alzheimer disease (AD) have prioritized variants in genes related to the amyloid cascade, lipid metabolism, and neuroimmune modulation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Survivors of childhood cancer are prone to neurocognitive impairment and premature aging, raising concerns about early onset dementia. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Epigenetic control of enhancers alters neuronal functions and may be involved in Alzheimer's disease (AD). 2 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
The molecular signatures of cells in the brain have been revealed in unprecedented detail, yet the ageing-associated genome-wide expression changes that may contribute to neurovascular dysfunction in neurodegenerative diseases remain elusive. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Type 2 diabetes is an established risk factor for dementia. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Affinity-based proteomics has enabled scalable quantification of thousands of protein targets in blood enhancing biomarker discovery, understanding of disease mechanisms, and genetic evaluation of drug targets in humans through protein quantitative trait loci (pQTLs). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lipid droplets are dynamic cellular organelles that store neutral lipids and coordinate metabolic and stress-response pathways. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies (GWAS) have identified more than 40 loci associated with Alzheimer's disease (AD), but the causal variants, regulatory elements, genes and pathways remain largely unknown, impeding a mechanistic understanding of AD pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Polygenic Risk Scores (PRS) for AD offer unique possibilities for reliable identification of individuals at high and low risk of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are overlapping, fatal neurodegenerative disorders in which the molecular and pathogenic basis remains poorly understood. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Activation of microglia is a prominent pathological feature in tauopathies, including Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The role of microglia cells in Alzheimer's disease (AD) is well recognized, however their molecular and functional diversity remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Single-cell RNA-sequencing (scRNA-Seq) is widely used to reveal the heterogeneity and dynamics of tissues, organisms, and complex diseases, but its analyses still suffer from multiple grand challenges, including the sequencing sparsity and complex differential patterns in gene expression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Large studies (e.g. UK Biobank) are increasingly used for GWAS and Mendelian randomization (MR) studies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) pathology has been increasingly explored through single-cell and single-nucleus RNA-sequencing (scRNA-seq & snRNA-seq) and spatial transcriptomics (ST). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The emergence of single nucleus RNA sequencing (snRNA-seq) offers to revolutionize the study of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Health risk factors such as body mass index (BMI) and serum cholesterol are associated with many common diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic association studies have identified 44 common genome-wide significant risk loci for late-onset Alzheimer's disease (LOAD). 3 key findings →
Evidence: low
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 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 →