27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
A reliable method of detecting Alzheimer disease (AD) in its prodromal state is needed for patient stratification in clinical trials or for personalizing existing or potential upcoming therapies. 4 key findings →
Design: cohort study Participants: 928 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In 272 participants, mean (SD) age was 70 (4.5) years, 270 were male (99.3%), and 83 (30.5%) were amyloid-PET positive. 5 key findings →
Design: cohort study Participants: 272 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Of 413 477 All of Us participants, 2038 were eligible. 5 key findings →
Design: cohort study Participants: 26 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study evaluates the quantile-aggregation method using both simulated data and publicly available Alzheimer disease randomized trial data. 1 key finding →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The study cohort included 245 patients with FTD (121 female [49.4%], 124 male [50.6%]; mean [SD] age, 65.2 [8.7] years), 2416 matched HCs (1190 female [49.3%], 1226 male [50.7%]; mean [SD] age, 65.0 [8.5] years), and 1326 patients with AD (777 female [58.6%], 549 male [41.4%]; mean [SD] age, 71.7 [9.8] years). 5 key findings →
Design: case-control study Participants: 245 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our data indicate that the APOE ε4 allele is an important predictor of cognitive function in PD across multiple domains. 5 key findings →
Participants: 1,079 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Eight single-nucleotide polymorphisms (false discovery rate P Conclusions and relevance Our findings demonstrate genetic overlap between AD and immune-mediated diseases and suggest that immune system processes influence AD pathogenesis and progression. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings enhance understanding of AD risk factors by relating validated susceptibility alleles to increased neuritic plaque pathology and implicate common genetic variation at the APP locus in the earliest, presymptomatic stages of AD. 4 key findings →
Participants: 114 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our results show that TREM2 is responsible for an unexpectedly high number of dementia cases in our cohort, suggesting that this gene should be taken into account when mutations in other dementia genes are excluded. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Poisson regression was used to model dementia incidence as a function of age, sex, educational level, race, and birth cohort, with profile likelihood used to identify the timing of significant increases or decreases in incidence. 3 key findings →
Participants: 1,348 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of 70 autopsied individuals (62 male, 8 female; mean [SD] age, 64.40 [13.94] years), 20 showed CTE-NC in the brain. 5 key findings →
Design: case-control study Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Available data, while limited and complicated by selection bias, indicate that exposure to RBT represents the greatest risk factor for CTE pathological features, although clinicopathological correlates and the nature of onset and progression of symptoms are largely unknown. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Such findings challenge the proposed sequence and suggest that Aβ-independent precursors underlie AD-typical neurodegenerative patterns. 3 key findings →
Design: cross-sectional Participants: 29 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Elevated cerebral Aβ level was associated with cholesterol fractions in a pattern analogous to that found in coronary artery disease. 5 key findings →
Design: cross-sectional Participants: 33 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among community-dwelling older adults, reports of shorter sleep duration and poorer sleep quality are associated with greater Aβ burden. 4 key findings →
Design: cross-sectional Participants: 70 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Microbleed presence was associated with lower CSF Aβ42 in AD and vascular dementia (standardized beta = -0.09, P = .003; standardized beta = -0.30, P = .01), and higher CSF tau in controls (standardized beta = 0.10, P = .03). 4 key findings →
Design: cross-sectional Participants: 914 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
These findings suggest that patterns of cortical Aβ and tau do not differ in people with PD-CN, people with PD-MCI, and healthy older adults. 5 key findings →
Design: cross-sectional Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this study, altered AQP4 expression was associated with aging brains. 4 key findings →
Participants: 79 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease in which microglia play a significant and active role. 4 key findings →
Participants: 923 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Age-associated changes in brain imaging and fluid biomarkers are characterized and compared in presenilin 1 (PSEN1)E280A mutation carriers and noncarriers from the world's largest known autosomal dominant Alzheimer disease (AD) kindred. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hexanucleotide repeat expansions in the chromosome 9 open reading frame 72 (C9orf72) gene underlie a significant fraction of frontotemporal dementia and amyotrophic lateral sclerosis. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Mutations in APP, PSEN1, and PSEN2 lead to early-onset Alzheimer disease (EOAD) but account for only approximately 11% of EOAD overall, leaving most of the genetic risk for the most severe form of Alzheimer disease unexplained. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This cohort study compares the risk of incident all-cause dementia among people with hearing loss who use vs do not use hearing aids. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The findings suggest that detection of αSyn oligomers by αSyn-PMCA in the CSF of patients affected by PD may offer a good opportunity for a sensitive and specific biochemical diagnosis of the disease. 5 key findings →
Participants: 76 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Similar to findings in adult mutation carriers, in the later preclinical and clinical stages of ADAD, mutation-carrying children were distinguished from control individuals by significantly higher plasma Aβ1-42 levels (mean [SD]: carriers, 18.8 [5.1] pg/mL and noncarriers, 13.1 [3.2] pg/mL; P Conclusions and relevance Children at genetic risk for ADAD have functional and structural brain changes and abnormal levels of plasma Aβ1-42. 2 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 →