27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Structured Abstract INTRODUCTION Adults with Down syndrome (DS) have a higher risk of developing Alzheimer’s disease (AD). 3 key findings →
Participants: 58 Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS), caused by trisomy 21, confers a near-universal risk for Alzheimer’s disease (AD), yet individuals exhibit marked variability in cognitive decline, suggesting the presence of cellular mechanisms that modulate vulnerability and resilience. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
MicroRNA dysregulation is implicated in neurodegenerative disorders, including Alzheimer’s disease (AD). 3 key findings →
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
The integrated stress response (ISR) is a highly conserved network essential for maintaining cellular homeostasis and cognitive function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Approximately 90% of Parkinson's disease (PD) patients exhibit olfactory deficits, which often precedes motor symptoms by years, and are a robust predictor for PD and subsequent cognitive decline. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging muscle showed increased inflammatory, extracellular-matrix, and stromal communication programs. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We introduce Dementia Language Models (DeLMs) – generalizable and controllable representations of cognitive impairment through language – alongside an evaluation framework for establishing their validity and clinical grounding. 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
Consequently, changes in mitochondrial DNA copy number (mtDNA-CN), the number of mtDNA genomes per cell or tissue sample, are associated with diseases ranging from cancer and obesity to psoriasis and all-cause mortality. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Sensitive human data underpin discoveries across medicine, biology and the social sciences, yet privacy regulation often prevents sharing them with collaborators or artificial intelligence (AI) systems. 1 key finding →
Evidence: moderate
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
Age-bias-corrected brain-age gap was most consistently associated with reduced diffusion-derived microstructural integrity and structural-network organization across cohorts. 2 key findings →
Design: longitudinal study Participants: 1,093 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Explainability methods applied to deep learning models for Alzheimer’s disease neuroimaging produce attribution maps that vary substantially across methods and architectures, yet no validated quantitative framework exists for determining which method most faithfully localises attribution signal within established AD neuroimaging biomarker anatomy at the individual subject level. 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
Insulin resistance is increasingly recognized as a metabolic factor associated with Alzheimer’s disease (AD); however, its relevance to hippocampal structural changes—a key pathological feature of AD—across disease stages is not fully understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
While loss of NMDA receptors (NMDARs) is associated with Alzheimer’s disease (AD) severity, the effect of sex or the relationship between regional NMDAR density and antemortem cognitive status across the AD spectrum has not been examined. 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 →