28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Overall, 1795 participants from Core and 1612 participants with at least one dose of lecanemab (Core + OLE) were included. 1 key finding →
Design: open-label trial Participants: 1,795 Evidence: high
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Of 236 eligible participants screened, 43 were excluded. 2 key findings →
Design: longitudinal study Participants: 142 Evidence: high
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Fifty-one AD patients enrolled, mean age 73.5. 4 key findings →
Design: clinical trial Evidence: high
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Clinical data supported a delayed onset of cognitive impairment in persons who were heterozygous for the APOE3 Ch variant in a kindred with a high prevalence of autosomal dominant Alzheimer's disease. 3 key findings →
Design: cohort Participants: 1,077 Evidence: moderate
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Differential diagnosis of dementia remains a challenge in neurology due to symptom overlap across etiologies, yet it is crucial for formulating early, personalized management strategies. 1 key finding →
Participants: 51,269 Evidence: low
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US clinical practice guidelines for the diagnostic evaluation of cognitive impairment due to Alzheimer's disease (AD) or AD and related dementias (ADRD) are decades old and aimed at specialists. 5 key findings →
Design: systematic-review Evidence: high
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In this 3-year randomized clinical trial, ω-3 treatment was safe and well-tolerated but failed to reach significant reductions in WML accumulation or neuronal integrity breakdown among all participants, which may be attributable to sample size limitations. 5 key findings →
Participants: 102 Evidence: high
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Brain clocks, which quantify discrepancies between brain age and chronological age, hold promise for understanding brain health and disease. 4 key findings →
Participants: 5,306 Evidence: low
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This study aimed to evaluate the impact of APOE4 homozygosity on Alzheimer's disease (AD) by examining its clinical, pathological and biomarker changes to see whether APOE4 homozygotes constitute a distinct, genetically determined form of AD. 2 key findings →
Participants: 3,297 Evidence: low
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Alzheimer's disease is the leading cause of dementia worldwide, but the cellular pathways that underlie its pathological progression across brain regions remain poorly understood 1-3 . 4 key findings →
Participants: 48 Evidence: low
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Baseline plasma VEGFA and PGF each showed a significant interaction with amyloid burden on prospective cognitive decline. 5 key findings →
Design: longitudinal study Participants: 317 Evidence: moderate
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Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease. 3 key findings →
Design: cohort study Participants: 137 Evidence: moderate
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The study consisted of 20 400 patients (9264 female [45.4%]; 1576 Black [7.7%], 3944 Latinx [19.3%], and 10 480 White [51.4%]), including 5100 patients with mTBI (median [IQR] age, 36.0 [25.0-51.0] years), 5100 patients with msTBI (median [IQR age, 35.0 [25.0-52.0] years), and 10 200 matched patients in the control group (median [IQR] age, 36.0 [25.0-51.0] years). 5 key findings →
Design: cohort study Participants: 400 Evidence: moderate
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There were 132 720 unique adults with Down syndrome from 2011 to 2019: 79 578 (53.2%) were male, 17 090 (11.7%) were non-Hispanic Black, 20 777 (15.7%) were Hispanic, 101 120 (68.8%) were non-Hispanic White, and 47 692 (23.3%) had ever had an Alzheimer dementia diagnosis. 3 key findings →
Design: cohort study Participants: 132 Evidence: moderate
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Our pilot studies (National Institutes of Health [NIH] stage 1A) have shown that MHB is feasible, acceptable, and associated with improvement in lifestyle behavior and cognitive outcomes. 4 key findings →
Design: randomized controlled trial Participants: 225 Evidence: high
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Disease-modifying therapies for Alzheimer's disease (AD) are likely to be most beneficial when initiated in the presymptomatic phase. 2 key findings →
Design: cross-sectional Participants: 567 Evidence: moderate
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Adults with Down syndrome demonstrate striatum-first amyloid accumulation with [ 11 C]PiB PET imaging, which has not been replicated with [ 18 F]florbetapir (FBP). 4 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A summary measure of γ-secretase activity (γ-secretase composite [GSC]) was calculated for each variant and compared with clinical history-derived AAO using correlation analyses. 3 key findings →
Design: cross-sectional Participants: 190 Evidence: moderate
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Of 4413 individuals (mean [SD] age, 71.27 [4.66] years, 2617 women [59.3%]), mean Aβ-PET was elevated in individuals with history of memory impairment in both parents (n = 455; mean [SD] standardized uptake value ratio [SUVR] = 1.12 [0.19]; Wilcoxon P = 1.1 × 10-5) and in those with only maternal history (n = 1772; mean [SD] SUVR = 1.10 [0.19]; Wilcoxon P = 2.70 × 10-5) compared with those with only paternal history (n = 632; mean [SD] SUVR = 1.08 [0.18]; Wilcoxon P = 1.1 × 10-5) or no family history (n = 1554; mean [SD] SUVR = 1.08 [0.19]; Wilcoxon P = 1.1 × 10-5). 3 key findings →
Design: cross-sectional Participants: 455 Evidence: high
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In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. 5 key findings →
Evidence: low
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The results underscore the impact of education on brain structure and function in LA, highlighting the importance of incorporating educational factors into diagnosing, care, and prevention, and emphasizing the need for global diversity in research. 5 key findings →
Participants: 1,412 Evidence: low
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Phase 3 (NIH stage 1B) is a feasibility randomized controlled trial of the intervention versus the Health Education Program control. 2 key findings →
Design: randomized controlled trial Participants: 28 Evidence: high
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Two of every three persons living with dementia reside in low- and middle-income countries (LMICs). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Disease staging, whereby the spatial extent and load of brain pathology are used to estimate the severity of Alzheimer disease (AD), is pivotal to the gold-standard neuropathological diagnosis of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our results reveal a spatial association between the epileptogenic focus and tau deposition, amyloid deposition, and neurodegeneration in early clinical stages of AD. 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.
1,034 records (3.6% 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 →