27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
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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These results do not support the hypothesis that celecoxib or naproxen prevent Alzheimer dementia, at least within the early years after initiation of treatment. 2 key findings →
Evidence: high
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Use of naproxen or celecoxib did not improve cognitive function. 2 key findings →
Design: longitudinal study Evidence: high
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Use of NSAIDs was associated with a lower risk of dementia (adjusted hazard ratio or aHR 0.76, 95% CI or CI 0.60-0.96) and, in particular, AD (aHR 0.63, CI 0.45-0.88), but not VaD (aHR 0.92, CI 0.65-1.28). 3 key findings →
Design: cohort study Participants: 3,229 Evidence: moderate
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Association of HT use and risk of AD may depend on timing of use. 4 key findings →
Design: randomized controlled trial Evidence: high
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Classification resulted in 227 persons with prevalent dementia at entry into the study and 480 incident cases during follow-up. 4 key findings →
Design: cohort study Participants: 227 Evidence: moderate
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Naproxen may attenuate cognitive decline in slow decliners while accelerating decline in fast decliners. 2 key findings →
Participants: 2,388 Evidence: low
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Enrollment began in March 2001 and ended in December 2004 when treatments were suspended because of concerns regarding cardiovascular safety of the treatments. 1 key finding →
Evidence: high
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Based on analysis of prospective and nonprospective studies, NSAID exposure was associated with decreased risk of Alzheimer's disease. 3 key findings →
Design: meta-analysis Evidence: high
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Long-term NSAID use may reduce the risk of AD, provided such use occurs well before the onset of dementia. 2 key findings →
Participants: 104 Evidence: high
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In this cohort study, statin therapy was not associated with a decreased risk of dementia. 5 key findings →
Design: cohort study Participants: 2,798 Evidence: moderate
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On the basis of their findings in this large community population of elderly people, the authors conclude that a wide range of dementia-associated mental and behavioral disturbances afflict the majority of individuals with dementia. 3 key findings →
Participants: 5,092 Evidence: low
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Participants were most likely to develop depression, apathy, or anxiety, and least likely to develop elation or disinhibition. 1 key finding →
Design: longitudinal study Evidence: moderate
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The APOE epsilon4 allele acts as a potent risk factor for AD by accelerating onset. 1 key finding →
Design: longitudinal study Participants: 3,308 Evidence: moderate
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Although statin use might be less frequent in those with prevalent dementia, we found no association between statin use and subsequent onset of dementia or AD. 3 key findings →
Design: cross-sectional Participants: 4,895 Evidence: low
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The data do not support an association between serum total cholesterol or high density lipoprotein in late life and subsequent risk of dementia or Alzheimer disease (AD). 5 key findings →
Design: cohort study Evidence: moderate
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Prior HRT use is associated with reduced risk of AD, but there is no apparent benefit with current HRT use unless such use has exceeded 10 years. 5 key findings →
Evidence: low
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These results do not support claims for the efficacy of nizatidine in over-the-counter dosages as a means of preventing symptom progression in AD. 2 key findings →
Evidence: high
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Commonly used organophosphate and organochlorine pesticides inhibit acetylcholinesterase at synapses in the somatic, autonomic, and central nervous systems and may therefore have lasting effects on the nervous system. 2 key findings →
Evidence: low
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Vascular disease in the brain is prevalent among incident dementia cases. 1 key finding →
Participants: 3,375 Evidence: low
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In participants with no epsilon4 alleles, the age-specific prevalence of AD reached a maximum and then declined after age 95. 3 key findings →
Evidence: low
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Parental death during childhood is associated with higher prevalence of AD, with different critical periods for father's versus mother's death, with strength of these associations attenuated by remarriage of the widowed parent. 5 key findings →
Participants: 4,108 Evidence: low
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The apoE epsilon 4 allele may be associated with decreased cognitive function in discordant twin pairs. 5 key findings →
Evidence: low
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Nonresponders in community surveys of the elderly appear to be disproportionately cognitively impaired. 3 key findings →
Design: cross-sectional Evidence: low
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The authors, a group of investigators with extensive research and clinical experience related to both late-life depression and Alzheimer disease (AD), propose provisional affective and behavioral inclusion and exclusion diagnostic criteria for Depression of AD.
Evidence: low
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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 →