27,380 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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Trial registration clinicaltrials.gov Identifier: NCT00056225. 1 key finding →
Participants: 340 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
A low-dose regimen of prednisone is not useful in the treatment of AD. 3 key findings →
Participants: 138 Evidence: high
Full summary, score breakdown and related studies → Original source
Antibody administration was well tolerated with doses up to 400 mg weekly. 2 key findings →
Design: clinical trial Participants: 52 Evidence: high
Full summary, score breakdown and related studies → Original source
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
In moderate stages of amnestic mild cognitive impairment, common cognitive tests provide better predictive accuracy than measures of whole brain, ventricular, entorhinal cortex, or hippocampal volumes for assessing progression to Alzheimer disease. 1 key finding →
Participants: 129 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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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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155 (85%) patients completed the trial (78 [88%] in dimebon group, 77 [82%] in placebo group). 5 key findings →
Participants: 89 Evidence: low
Full summary, score breakdown and related studies → Original source
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
Full summary, score breakdown and related studies → Original source Free full text
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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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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A previous report describes decreased decline in ADAS-cog (delta = 3.1, p = 0.008 at 18 months, ANCOVA with multiple imputation), relative to placebo, following a 5 mg/day dose of TTP488. 4 key findings →
Design: clinical trial Participants: 399 Evidence: high
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As a potential disease-modifying treatment for Alzheimer disease (AD), 3-amino-1-propanesulfonic acid (3APS) is a compound that binds to amyloid beta (Abeta), a toxic protein known to aggregate, leading to amyloid plaque deposition in the brain. 4 key findings →
Design: open-label trial Participants: 58 Evidence: high
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The results of this study indicate that rofecoxib or low-dose naproxen does not slow cognitive decline in patients with mild-to-moderate AD. 5 key findings →
Participants: 474 Evidence: high
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Of 44 844 patients invited to the APT Webstudy, the mean (SD) age was 64.7 (10.1) years, 25 447 (56.8%) were women, 25 044 (55.8%) had Medicaid insurance, 11 347 (25.3%) were Hispanic/Latino, 9526 (21.2%) were non-Hispanic Asian, 6044 (13.5%) were non-Hispanic Black, and 12 109 (27%) were non-Hispanic White. 2 key findings →
Participants: 844 Evidence: high
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(1) Data-driven AD progression models supported multifactorial interactions rather than a linear cascade of events. 4 key findings →
Design: longitudinal study Evidence: high
Full summary, score breakdown and related studies → Original source
Interventions that have even quite modest effects at the individual level could drastically reduce the future burden of dementia associated with Alzheimer's disease at the population level. 1 key finding →
Evidence: high
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Participants age 60-85 years deemed cognitively unimpaired were disclosed an elevated or not elevated brain amyloid result by a certified clinician. 5 key findings →
Participants: 3,686 Evidence: high
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Patients with MCI had a predominant memory impairment with relative sparing of other cognitive domains and were intermediate between clinically normal individuals and patients with AD on cognitive and functional ratings. 3 key findings →
Participants: 769 Evidence: low
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ADNI-3 will aim to inform AD treatment trials and facilitate development of AD disease-modifying treatments. 2 key findings →
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 →