27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloid-related imaging abnormalities (ARIA) in the form of edema/effusions (ARIA-E) or hemorrhagic lesions (ARIA-H) are the most impactful adverse event associated with anti-amyloid immunotherapy for Alzheimer disease. 1 key finding →
Evidence: low
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Adults with Down syndrome carry high risk of developing Alzheimer’s disease and efforts to include this population in clinical trials remain limited. 4 key findings →
Design: longitudinal study Participants: 237 Evidence: moderate
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Since its first description in 1906 by Dr. Alois Alzheimer, Alzheimer’s disease (AD) has been the most common type of dementia. 4 key findings →
Evidence: low
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By age 40 years over 90% of adults with Down syndrome (DS) have Alzheimer’s disease (AD) pathology and most progress to dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is a heterogeneous disease with many genes are associated with AD risk. 4 key findings →
Participants: 360 Evidence: low
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Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217. 4 key findings →
Participants: 484 Evidence: low
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We estimated associations of educational attainment and Alzheimer disease genetic risk with treatment initiation and incident dementia and compared GLP-1 receptor agonist initiators with initiators of non-sodium-glucose cotransporter 2 inhibitor second-line therapies, with a separate sodium-glucose cotransporter 2 inhibitor compa 4 key findings →
Design: cohort study Participants: 14,364 Evidence: moderate
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Anti-amyloid immunotherapy is used to treat Alzheimer disease (AD) with moderate benefits and potentially serious side effects due to amyloid related imaging abnormality with effusions/edema (ARIA-E). 4 key findings →
Design: cross-sectional Evidence: low
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It is estimated that for people aged 65 years and older, the risk of developing Alzheimer’s disease was nearly double for women compared with men (Weinstein et al., 2012). 5 key findings →
Evidence: low
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INTRODUCTIONNovel capillary-blood collection methods have not yet been evaluated for a wide range of central nervous system (CNS) and neurodegenerative disease-related proteins. 2 key findings →
Evidence: low
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Alzheimers disease (AD) is defined by progressive neurodegeneration, yet a substantial fraction of its genetic risk maps to non-neuronal processes. 1 key finding →
Evidence: low
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Examples include subpopulations of CD4+ T cells associated with inflammatory bowel disease, characterized by enrichment for a multi-cytokine phenotype and overlap with the naive NF-kB-activated, central memory, and effector memory CD4+ T subtypes, and subpopulations of microglia associated with Alzheimers disease, characterized by depletion of homeostatic programs and localization to the midtemporal gyrus, dorsolateral prefrontal cortex, and medial entorhinal cortex. 3 key findings →
Evidence: low
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ImportanceThe ASPREE randomized trial found no overall benefit of low-dose aspirin for disability-free survival among older adults. 4 key findings →
Design: randomized controlled trial Evidence: high
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Spatial omics enables the integration of high-dimensional molecular organization with clinical outcomes, yet incorporating spatial single-cell information into predictive models at the population scale remains challenging. 1 key finding →
Evidence: moderate
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INTRODUCTIONSleep-dependent memory consolidation is impaired early in Alzheimers disease (AD). 2 key findings →
Participants: 37 Evidence: high
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IntroductionFrontotemporal lobar degeneration (FTLD) is a devastating disease that commonly results in early onset dementia, yet its rarity and heterogeneity limit large-scale research and clinical trials. 2 key findings →
Design: longitudinal study Participants: 567 Evidence: moderate
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For TabCAT tests, there were no notable floor or ceiling effects, and test scores were associated with age and education as expected. 3 key findings →
Design: cohort study Participants: 563 Evidence: moderate
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Plasma p-tau217 concentrations were positively associated with plasma TNF- (Kendalls {tau} = 0.339; P < .001) and IL-6 (Kendalls {tau} = 0.310; P < .001) concentrations. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →