The primary efficacy analysis did not show cognitive benefit with huperzine A 200 μg BID. 3 key findings →
Participants: 70 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The primary efficacy analysis did not show cognitive benefit with huperzine A 200 μg BID. 3 key findings →
Participants: 70 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Despite evidence of target engagement as indicated by an increase in serum insulin-like growth factor-1, the human growth hormone secretagogue MK-677 25 mg was ineffective at slowing the rate of progression of Alzheimer disease. 2 key findings →
Participants: 563 Evidence: high
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Ladostigil was safe and well tolerated but did not delay progression to dementia. 3 key findings →
Design: clinical trial Participants: 107 Evidence: high
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Overall, we showed that SDB was associated with MTL atrophy in cognitively asymptomatic older adults engaged in the Alzheimer continuum, which may increase the risk of developing memory impairment over time. 3 key findings →
Design: randomized controlled trial Participants: 122 Evidence: high
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Classification of evidence This study provides Class II evidence that specific dual-task training improves dual-task performance during walking under complex S3 conditions in geriatric patients with mild to moderate dementia. 3 key findings →
Evidence: high
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It has been assumed that each MCI subtype is associated with an increased risk for a particular type of dementia. 2 key findings →
Design: longitudinal study Evidence: moderate
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Dementia is a key part of survival in Parkinson disease and must be planned for in services for this condition. 1 key finding →
Design: cohort study Participants: 140 Evidence: moderate
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The failure of selective cyclo-oxygenase-2 inhibition to slow the progression of AD may indicate either that the disease process is too advanced to modify in patients with established dementia or that cyclo-oxygenase-2 does not play a significant role in the pathogenesis of the disorder. 5 key findings →
Participants: 692 Evidence: low
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In this community-based cohort without dementia, florbetapir uptake is associated with older age and APOE genotype. 5 key findings →
Design: longitudinal study Participants: 329 Evidence: moderate
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In the 1990 subcohort (25,696 person-years), 286 persons developed dementia, and in the 2000 subcohort (8,384 person-years), 49 persons. 4 key findings →
Design: cohort study Participants: 5,727 Evidence: moderate
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We systematically searched PubMed for eligible studies reporting data on CSF biomarkers reflecting amyloid precursor protein metabolism (Aβ42, Aβ40), neurodegeneration (t-tau), and tangle pathology (p-tau) in symptomatic sporadic CAA cohorts vs controls and patients with Alzheimer disease (AD). 4 key findings →
Design: meta-analysis Participants: 59 Evidence: high
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There is a clear need to characterize and validate molecular biomarkers of cerebral amyloid angiopathy (CAA), in an effort to improve diagnostics, especially in the context of patients with Alzheimer disease (AD) receiving immunotherapies (for whom underlying CAA is the driver of amyloid-related imaging abnormalities). 4 key findings →
Design: meta-analysis Participants: 289 Evidence: high
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The PubMed and Embase databases were searched for clinical trials of anti-Aβ immunotherapy published on or before January 12, 2022. 4 key findings →
Design: clinical trial Participants: 9,429 Evidence: high
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In this multinational, randomized, double-blind, placebo-controlled, parallel-group clinical trial, 788 patients with probable VaD who also satisfied strict centrally read MRI criteria were randomized to receive galantamine or placebo. 4 key findings →
Participants: 788 Evidence: high
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MoCA was administered to 274 patients from 2 prospective hospital-based cohort studies in Germany (n = 125) and France (n = 149). 4 key findings →
Design: cohort study Participants: 125 Evidence: moderate
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In this single-center observational study, we included all individuals who visited the Alzheimer Center Amsterdam and had a clinical diagnosis of subjective cognitive decline (SCD), mild cognitive impairment (MCI), or probable AD dementia and were A+. 4 key findings →
Design: longitudinal study Participants: 520 Evidence: moderate
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In an elderly population of Southern Italy with a typical Mediterranean diet, high MUFA intakes appeared to be protective against age-related cognitive decline. 2 key findings →
Design: longitudinal study Participants: 704 Evidence: high
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Hypertension after age 65 years is not associated with AD and does not adversely affect memory, language, or general cognitive function. 5 key findings →
Design: longitudinal study Participants: 1,259 Evidence: moderate
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In the absence of clinical stroke, people with incident atrial fibrillation are likely to reach thresholds of cognitive impairment or dementia at earlier ages than people with no history of atrial fibrillation. 2 key findings →
Design: longitudinal study Participants: 5,150 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In a study of nearly 190,000 older US military veterans, those who had experienced a traumatic brain injury were about 57% more likely to develop dementia over the next 9 years than veterans without a brain injury history. 4 key findings →
Design: cohort Participants: 188,764 Evidence: high
Full summary, score breakdown and related studies → Original source
At baseline, 2,279 dementia-free participants with available blood samples were included (median age 72 (interquartile range, 61-81) years; 62% female). 4 key findings →
Design: cohort Participants: 2,279 Evidence: moderate
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These results suggest that increasing levels of tau most consistently relate to declines in cognition preceding biomarker collection. 4 key findings →
Design: longitudinal study Participants: 152 Evidence: moderate
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SUVr abnormality was most frequently observed in cingulate, followed by orbitofrontal, precuneal, and insular cortices and then the associative, temporal, and occipital regions. 1 key finding →
Design: longitudinal study Participants: 867 Evidence: moderate
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The clinical diagnosis of probable AD dementia demonstrated good agreement with biologically defined AD (positive predictive value 85.2%). 3 key findings →
Design: cohort study Participants: 166 Evidence: moderate
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In a community-based cohort of 70-year olds, P-NfL was associated with both prevalent and incident CKD, while CSF and/or imaging measures did not differ by CKD status. 3 key findings →
Design: cohort study Participants: 744 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. 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 →