28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The drug did not prevent clinical progression in a trial involving patients with mild-to-moderate dementia due to Alzheimer's disease. 4 key findings →
Participants: 1,454 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is a progressive, irreversible, and fatal disease for which accumulation of amyloid beta is thought to play a key role in pathogenesis. 4 key findings →
Design: clinical trial Participants: 1,638 Evidence: high
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Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate Alzheimer's disease and was associated with treatment-related adverse events. 3 key findings →
Participants: 1,958 Evidence: high
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Trial registration clinicaltrials.gov Identifier: NCT00056225. 1 key finding →
Participants: 340 Evidence: high
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Significant proportions of the observed variance in age at symptom onset in ADAD can be explained by family history and mutation type, providing empirical support for use of these data to estimate onset in clinical research. 2 key findings →
Participants: 3,275 Evidence: low
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Simvastatin had no benefit on the progression of symptoms in individuals with mild to moderate AD despite significant lowering of cholesterol. 4 key findings →
Participants: 406 Evidence: high
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The primary planned analyses did not show a significant treatment effect, but were confounded by unexplained variance. 5 key findings →
Design: randomized controlled trial Participants: 1,052 Evidence: high
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Compared with participants who learned that they had a not elevated amyloid result, individuals who learned of an elevated amyloid result were no more likely to experience short-term increases in depression (mean [SD] change in the Geriatric Depression Scale score, 0.02 [1.3] vs 0.04 [1.3]; P = .90), anxiety (mean [SD] change in State-Trait Anxiety Inventory score, -0.02 [3.2] vs -0.15 [3.0]; P = .65), or suicidality (mean [SD] change in the Columbia Suicide Severity Rating Scale score, 0.0 [0.4] vs -0.01 [0.5]; P = .67). 5 key findings →
Design: cohort study Participants: 1,167 Evidence: high
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change from baseline in Preclinical Alzheimer Cognitive Composite score. 5 key findings →
Participants: 189 Evidence: high
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Among the 445 participants (243 with normal amyloid, 202 with elevated amyloid), mean (SD) age was 74.0 (5.9) years, mean education was 16.4 (2.7) years, and 52% were women. 2 key findings →
Design: longitudinal study Participants: 243 Evidence: moderate
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Patients with MCI converted to AD at an annual rate of 17.2%. 2 key findings →
Design: longitudinal study Participants: 85 Evidence: moderate
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There were no baseline differences between active treatment and placebo groups in age, education, brain volumes, clinical rating scores, or APOE ε4 carrier status. 3 key findings →
Participants: 313 Evidence: high
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The pathophysiological process of Alzheimer's disease (AD) is thought to begin many years before the diagnosis of AD dementia. 5 key findings →
Design: longitudinal study Evidence: moderate
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Levels of plasma p-tau217 increased significantly in Aβ+ participants before showing significant deceleration (χ2 = 21.7; P Conclusions and relevance This study found that tau PET is valuable for both prognostic and real-time tracking of disease progression. 2 key findings →
Design: cohort Participants: 1,707 Evidence: moderate
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This multicenter randomized clinical trial demonstrated the feasibility of sham-surgery-controlled stereotactic gene delivery studies in patients with AD. 3 key findings →
Design: clinical trial Participants: 49 Evidence: high
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PF-04494700 at 20 mg/d was associated with increased adverse events and cognitive decline. 3 key findings →
Participants: 399 Evidence: high
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) is an ongoing, longitudinal, multicenter study designed to develop clinical, imaging, genetic, and biochemical biomarkers for the early detection and tracking of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 400 Evidence: moderate
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The Alzheimer's Disease Neuroimaging Initiative has successfully recruited cohorts of cognitively normal subjects, subjects with mild cognitive impairment (MCI), and subjects with Alzheimer disease with anticipated baseline characteristics. 1 key finding →
Participants: 819 Evidence: low
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The efficacy, safety and disease-modification of tramiprosate (homotaurine)were investigated in a recently completed large-scale Phase III clinical study in patients with mild to moderate Alzheimer's disease (AD), the Alphase study. 4 key findings →
Design: longitudinal study Participants: 109 Evidence: high
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Ten weeks of treatment with PF-04494700 was safe and well tolerated in patients with mild-to-moderate Alzheimer disease, indicating the feasibility of a larger long-term efficacy trial. 3 key findings →
Participants: 28 Evidence: high
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At 48 months, group differences between clinical progressors and non-progressors were significant for self (2.13, SE=0.45, P Conclusions and relevance Demonstrating long-term clinical benefit will be critical for the success of recently launched secondary prevention trials. 1 key finding →
Design: longitudinal study Participants: 468 Evidence: moderate
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Previous studies of Aβ plasma as a biomarker for Alzheimer's disease (AD) obtained conflicting results. 5 key findings →
Design: longitudinal study Participants: 715 Evidence: moderate
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In ADNI, Aβ-positive participants showed more decline than did Aβ-negative participants with regard to the ADCS-PACC score at 24 months (mean [SE] difference, -1.239 [0.522] [95% CI, -2.263 to -0.215]; P = .02). 4 key findings →
Evidence: low
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There were no statistical differences between the placebo or solanezumab groups in CDR-G, CDR-SB, specific CDR boxes or CDR composite scores over the course of the trial. 3 key findings →
Participants: 583 Evidence: high
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These studies fundamentally deepen our understanding of AD progression and its underlying genetic basis, which in turn informs and improves clinical trial design. 2 key findings →
Design: longitudinal study Evidence: moderate
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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.
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 (3.7% 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 →