28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
APOE epsilon 4 may influence rate of cognitive decline most significantly in the earliest stages of Alzheimer disease. 3 key findings →
Design: cohort study Evidence: moderate
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This advantage may represent a sex-specific form of cognitive reserve delaying verbal memory decline until more advanced disease stages. 1 key finding →
Design: cross-sectional Participants: 379 Evidence: low
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A significant portion of sleep-disordered breathing is associated with ApoE epsilon4 in the general population. 4 key findings →
Design: cohort study Evidence: moderate
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The influence of this genetic risk may begin in early life and make an individual more susceptible to cognitive impairment in late life. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
While prior work reliably demonstrates that the APOE ɛ4 allele has deleterious group level effects on Alzheimer disease pathology, the homogeneity of its influence across the lifespan and spatially in the brain remains unknown. 1 key finding →
Design: longitudinal study Evidence: moderate
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In this review, the evidence that single clinically defined cardiovascular risk factors are significantly associated with incident AD is inconsistent at best. 2 key findings →
Design: systematic review Evidence: high
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Alzheimer disease pathologic changes are common in DLB and are associated with the clinical phenotype. β-Amyloid is associated with cognitive impairment, and tau pathology is associated with lower frequency of clinical features of DLB. 5 key findings →
Participants: 417 Evidence: moderate
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The genotype KL-VSHET+ is associated with reduced AD risk and Aβ burden in individuals who are aged 60 to 80 years, cognitively normal, and carrying APOE4. 5 key findings →
Design: case-control study Participants: 20 Evidence: moderate
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Using parametric methods, no evidence for linkage to the region spanned by the chromosome 12 markers could be detected if familial AD is assumed to arise from the same genetic locus in all 53 families. 2 key findings →
Design: cohort study Participants: 173 Evidence: moderate
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Among the 183 study participants, mean (SD) age was 85.5 (3) years, 76 were women (41.5%), and 177 were white (96.7%). 4 key findings →
Design: cross-sectional Participants: 183 Evidence: low
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After the change point, carriers had a statistically significant cognitive decline with a loss of 0.24 (95% CI, -0.26 to -0.22) points per year for the word list recall test and 2.13 (95% CI, -2.29 to -1.96) points per year for total scores. 5 key findings →
Design: cohort study Participants: 493 Evidence: moderate
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This preliminary report suggests that CETP V405 valine homozygosity is associated with slower memory decline and lower incident dementia and AD risk. 5 key findings →
Design: cohort study Participants: 523 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Indeed, in our review, we observed a stage-dependent neuroinflammatory process in the AD brain. 2 key findings →
Design: longitudinal study Evidence: moderate
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Research into dementia prevention is of paramount importance if the dementia epidemic is to be halted. 5 key findings →
Evidence: high
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Atorvastatin therapy may be of benefit in the treatment of mild-to-moderately affected AD patients, but the level of benefit produced may be predicated on earlier treatment, an individual's apolipoprotein E genotype or whether the patient exhibits elevated cholesterol levels. 3 key findings →
Evidence: high
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The protective effect of statin on Alzheimer disease (AD) is still controversial, probably due to the debate about when to start the use of statin and the lack of any large-scale randomized evidence that actually supports the hypothesis. 2 key findings →
Design: randomized controlled trial Evidence: high
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A 2-hour infusion of 0.1 to 10 mg/kg ponezumab was well tolerated in subjects with mild-to-moderate AD. 4 key findings →
Evidence: high
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Sensitivity to psychotropic medications presents a therapeutic challenge when treating neuropsychiatric symptoms in patients with dementia with Lewy bodies (DLB). 3 key findings →
Evidence: high
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In this study, Triflusal therapy was associated with a significant lower rate of conversion to dementia that is likely to be clinically relevant. 5 key findings →
Evidence: high
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A plethora of reports suggest that copper (Cu) homeostasis is disturbed in Alzheimer's disease (AD). 4 key findings →
Design: clinical trial Evidence: high
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These findings do not provide evidence of improvement in behavioral symptoms, functional status, or QoL of hearing impaired AD patients and their caregivers after 6 months of HA use. 4 key findings →
Evidence: high
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Milacemide does not appear to be an effective treatment in enhancing cognition in SDAT patients. 2 key findings →
Participants: 113 Evidence: high
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These estimates suggest that DSS provides clinically important reductions in symptoms of AD and VD and can be a promising anti-dementia drug candidate. 5 key findings →
Design: systematic review Participants: 567 Evidence: high
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This study indicates no benefits for memantine in the long-term treatment and prophylaxis of clinically significant neuropsychiatric symptoms. 5 key findings →
Participants: 199 Evidence: high
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At baseline, there were no statistically significant differences in demographic characteristics and in outcome variables (HHI, GSES, and SF-12v2 mental component score and physical component score) between users and nonusers. 5 key findings →
Design: randomized controlled trial Participants: 101 Evidence: high
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 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 →