27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Untargeted mass spectrometry remains underutilised for blood-based biomarker discovery in dementia research from large cohorts, where affinity-based approaches dominate. 3 key findings →
Participants: 14,258 Evidence: low
Full summary, score breakdown and related studies → Original source
Across all cases, the SNCA association was indexed by a 5′ signal previously associated with dementia with Lewy bodies and rapid eye movement sleep behaviour disorder, rather than the canonical 3′ Parkinson’s disease variant. 4 key findings →
Design: meta-analysis Participants: 1,362 Evidence: high
Full summary, score breakdown and related studies → Original source
This study represents the largest PD AAO meta-analysis in European-ancestry populations to date. 5 key findings →
Design: meta-analysis Participants: 50,859 Evidence: high
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases (NDDs) are driven by multiple related yet distinct pathological processes that evolve over decades, resulting in substantial clinical and neuropathological heterogeneity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Polygenic risk scores (PRSs) have improved substantially in predictive performance, yet results remain difficult to compare across studies that differ in cohorts, phenotype definitions, and evaluation procedures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sequence models predict the molecular effects of genetic variation, yet their contribution to interpreting Alzheimer’s disease (AD) association signals remains uncertain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetically predicted BP raises WMH in European and Japanese ancestry. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Identifying early life biomarkers of suboptimal aging trajectories could help design interventions to delay or even prevent the onset of pathological conditions in older adulthood. 1 key finding →
Participants: 522 Evidence: low
Full summary, score breakdown and related studies → Original source
Inverse-variance weighted MR indicated that genetically predicted focal epilepsy with hippocampal sclerosis was associated with increased odds of AD (OR=3.99, 95% CI 1.17–13.61; P=0.027). 5 key findings →
Participants: 803 Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic pain and cognitive impairment are rising ageing-related burdens. 4 key findings →
Design: longitudinal study Participants: 387,649 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genetic risks were primarily associated with Aβ and tau pathology, clinical risks with neurodegeneration, and SDoH risks with cognition, suggesting that risk factors exert differential effects on AD pathophysiology. 5 key findings →
Design: cohort study Participants: 2,276 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
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
The two sites associated with interactions between AD and a metabolic condition could explain the influence that those conditions have on the risk for AD and are prime candidates for future study. 3 key findings →
Participants: 551 Evidence: moderate
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
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
Conventional, cohort-based staging exhibited profound topographical inversion, yielding negative correlations for TDP-43 ( ρ = -0.9113, p < 0.001) and α-synuclein ( ρ = -0.8660, p = 0.003) sub-cohorts. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The phenotypic measures “Slope” and “dMMSE/dt” consistently showed strong performance across a range of data distributions, while “Time-to-MMSE10” was particularly effective in cohorts with a higher proportion of individuals experiencing severe cognitive decline. 2 key findings →
Design: longitudinal study Participants: 500 Evidence: moderate
Full summary, score breakdown and related studies → Original source
MTHFR C677T homozygosity was independently associated with vascular dementia (OR 3.2; 95% CI 1.1–8.9; p=0.027) and showed clustering with cognitive impairment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The unsupervised machine learning pipeline successfully identified a composite genetic cluster that emerged as an influential predictor in terms of relative magnitude ( η p 2 ). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
8 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 8. The same 8 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 →