27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Polygenic scores summarise genetic predisposition to a trait, but a population-level accuracy figure cannot tell a clinician whether a given prediction is reliable for the person in front of them. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Age-related hearing loss is a leading modifiable risk factor for dementia and is increasingly recognized as a non-motor feature of Parkinson’s disease (PD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Partitioned-heritability studies have shown which tissues carry the heritability of complex traits, but whether the regulatory layer whose annotations are most informative for heritability within a tissue differs between traits has not been tested, because measured annotations for different layers come from different sets of biosamples. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Postmitotic neurons must preserve genome integrity for decades despite continuous oxidative, transcription-associated, and environmental DNA damage. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In brain, inverse-variance random-effects meta-analysis (DerSimonian–Laird) across six independent postmortem adult-brain GEO cohorts (GSE33000, GSE132903, GSE173955, GSE159699, GSE5281, GSE48350) yielded 458 analyzable panel genes, 167 at Benjamini–Hochberg FDR < 0.05, and 141 high-confidence genes (FDR < 0.05, measured in at least three cohorts, direction-concordant in at least 70% of cohorts, and nominally significant in at least two cohorts). 1 key finding →
Design: meta-analysis Participants: 329 Evidence: high
Full summary, score breakdown and related studies → Original source
Parkinson disease (PD) was examined in four primary adult-brain GEO cohorts (GSE49036, GSE20141, GSE8397, GSE7621) using a frozen 468-gene redox, metal, xenobiotic, and barrier panel. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
In this prospective birth cohort study, prenatal exposure to a persistent environmental toxicant was associated with lower plasma Aβ42/40 ratio and worse cognitive performance in midlife, consistent with DDE accelerating the preclinical trajectory of AD-related biological changes decades before symptom onset. 5 key findings →
Design: cohort study Participants: 179 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neuroticism, a personality trait characterized by the predisposition to experience intense and frequent negative emotions, has been associated with an increased risk of Alzheimer’s disease (AD). 5 key findings →
Participants: 1,277 Evidence: low
Full summary, score breakdown and related studies → Original source
INTRODUCTIONLittle is understood about the extent to which lifestyle factors can advance or delay the risk of developing dementia, and whether that is dependent on non-modifiable factors, e.g. sex and genetic susceptibility.METHODSAmong 224,516 UK Biobank participants aged ≥50 years at baseline, Cox regression examined the relations of apolipoprotein E gene (APOE) genotypes, and lifestyle with incident dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings demonstrate differential effects of nicotine on AD risk and smoking intensity on white matter integrity, requiring triangulation with complementary methodological approaches to better inform potential long-term risks of nicotine intake on neurocognitive outcomes. 3 key findings →
Design: cohort study Participants: 334,757 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, in which epitranscriptomic modifications, especially RNA methylation, may exert crucial regulatory effects. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ABCA7-KO iMGs were deficient for proteins involved in lysosome function, measured by down-regulated lysosomal proteomic signatures, as well as reduced DQ-BSA activity and reduced LAMP1+ area. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E ε4 (APOE4) allele is the strongest genetic risk factor for developing sporadic Alzheimer’s disease (AD), which accounts for the vast majority of AD cases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is characterised by aberrant amyloid beta and tau aggregation, neuroinflammation, demyelination and neurodegeneration, which have been linked to changes in cell-specific gene expression signatures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study demonstrated MMSE scores can be systematically extracted and curated from the VA EHR. 3 key findings →
Design: cross-sectional Participants: 49,555 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In SPRINT, intensive vs standard SBP control yielded a significantly larger 4-year absolute risk reduction in dementia among APOE ε4 carriers (−1.7%) than non-carriers (0.2%; P-interaction = .045); the relative-scale interactions were directionally consistent but not significant. 3 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source
We recommend using a broad (ADRD) algorithm without CMS or medication data, particularly for epidemiological studies or a strict AD algorithm including CMS and medication cases for genetic discovery of late-onset AD associations in VA EMR, and a strict AD algorithm without CMS data for applications focused solely on AD and sensitive to misspecification. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Multimodal integration of cognitive, neuroimaging, and polygenic data in the MHS-RWD tool yields strong discrimination for both early diagnosis of dementia and AD differential diagnosis. 2 key findings →
Participants: 1,100 Evidence: low
Full summary, score breakdown and related studies → Original source
Spontaneous speech acoustics capture p-tau217/APOE-defined AD risk despite preserved cognition, supporting speech as a scalable, biologically grounded biomarker for preclinical AD risk stratification. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified 27 phenotypes associated with APOE, mainly in neurological and lipid-related traits. 5 key findings →
Participants: 181,880 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Adults with Down syndrome (DS) develop Alzheimer’s disease (AD) brain pathology by age 40 due to triplication of the Amyloid Precursor Protein ( APP ) gene on chromosome 21. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down Syndrome (DS) is the most abundant genetic form of mental retardation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, and its incidence is rising rapidly with population aging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E ε4 ( APOE ε4) allele is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD), yet its associated protein changes across biofluids, brain regions, and cell types remain incompletely understood. 3 key findings →
Participants: 1,691 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Understanding how a stable structural connectome supports flexible cognition, especially in aging, is a fundamental question in neuroscience. 5 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 →