No significant differences were found in the primary efficacy analysis. 2 key findings →
Design: clinical trial Participants: 234 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
No significant differences were found in the primary efficacy analysis. 2 key findings →
Design: clinical trial Participants: 234 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among 1736 randomized participants (mean age, 73.0 years; 996 [57.4%] women; 1182 [68.1%] with low/medium tau pathology and 552 [31.8%] with high tau pathology), 1320 (76%) completed the trial. 3 key findings →
Design: clinical trial Participants: 860 Evidence: high
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Outcome measures were analyzed using repeated-measures analysis of covariance. 2 key findings →
Participants: 64 Evidence: high
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Of 54 adults assessed for eligibility, 11 did not meet study criteria, and 9 declined to participate. 2 key findings →
Participants: 34 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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Although prespecified criteria for testing treatment effects were not met, these data suggest a potential treatment effect in patients with mild AD treated with high-dose crenezumab. 4 key findings →
Design: clinical trial Participants: 184 Evidence: high
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Avagacestat did not demonstrate efficacy and was associated with adverse dose-limiting effects. 5 key findings →
Design: randomized controlled trial Participants: 263 Evidence: high
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In cognitively intact individuals at risk, sustained treatment with naproxen sodium 220 mg twice daily increases frequency of adverse health effects but does not reduce apparent progression of presymptomatic AD. 4 key findings →
Participants: 195 Evidence: high
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Based on the results of the prespecified coprimary endpoints, this study was negative. 5 key findings →
Design: clinical trial Participants: 624 Evidence: high
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A significant drug-placebo difference on the ADAS-Cog12 favoring GV-971 was present at each measurement time point, measurable at the week 4 visit and continuing throughout the trial. 3 key findings →
Design: clinical trial Participants: 818 Evidence: high
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In both phases, men were encouraged to visit their physician if the screen results indicated possible cognitive impairment. 3 key findings →
Design: cohort study Participants: 7,540 Evidence: high
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Is it possible to prevent atrophy of key brain regions related to cognitive decline and Alzheimer's disease (AD)? 3 key findings →
Evidence: high
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Previous Cochrane reviews have considered the use of cholinesterase inhibitors in both Parkinson's disease with dementia (PDD) and dementia with Lewy bodies (DLB). 4 key findings →
Participants: 1,236 Evidence: high
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This study reports the findings of the first large-scale Phase III investigator-driven clinical trial to slow the rate of cognitive decline in Alzheimer disease with a dihydropyridine (DHP) calcium channel blocker, nilvadipine. 4 key findings →
Participants: 577 Evidence: high
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At randomization, the mean age is 72, 50% female, 77% with CDR-global score 0.5, and mean MMSE score 23.8. 5 key findings →
Design: clinical trial Participants: 464 Evidence: high
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These data suggest a revision of the original ADAPT hypothesis that NSAIDs reduce AD risk, as follows: NSAIDs have an adverse effect in later stages of AD pathogenesis, whereas asymptomatic individuals treated with conventional NSAIDs such as naproxen experience reduced AD incidence, but only after 2 to 3 years. 5 key findings →
Participants: 54 Evidence: high
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Among older persons with AMD, oral supplementation with LCPUFAs or lutein/zeaxanthin had no statistically significant effect on cognitive function. 5 key findings →
Participants: 89 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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Of 200 participants, 99 were assigned to methylphenidate and 101 to placebo. 5 key findings →
Design: longitudinal study Participants: 200 Evidence: high
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We included randomized controlled trials (RCTs) and nonrandomized controlled studies at lower risk of bias comparing ChEI treatment with placebo or usual treatment, for 6 months or longer, in patients with dementia of any type. 5 key findings →
Design: systematic review Participants: 79,153 Evidence: high
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Of the 120 participants (mean age, 71.4 [SD, 8.6] years; 55% were female), 93 (77.5%) completed the trial. 1 key finding →
Design: phase-2-trial Participants: 120 Evidence: null result
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In participants with early symptomatic AD, zagotenemab failed to achieve significant slowing of clinical disease progression compared with placebo. 5 key findings →
Design: clinical trial Participants: 360 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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This study showed that subcutaneous etanercept (50 mg/wk) was well tolerated in this small group of patients with Alzheimer disease dementia, but a larger more heterogeneous group needs to be tested before recommending its use for broader groups of patients. 4 key findings →
Participants: 20 Evidence: high
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There was no difference in the age (mean [SD], 74.17 [7.96] years), sex (12 women [67%]), or baseline Mini-Mental State Examination score (mean [SD], 19.39 [3.24]) between the crossover (n = 9) and open-label groups (n = 9). 3 key findings →
Design: open-label trial Evidence: high
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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →