27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Bapineuzumab did not improve clinical outcomes in patients with Alzheimer's disease, despite treatment differences in biomarkers observed in APOE ε4 carriers. 1 key finding →
Design: clinical trial Participants: 1,090 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
1795 participants with early AD were enrolled in Clarity AD, of which 1521 were ApoE ε4 heterozygotes or non-carriers (85 %). 5 key findings →
Design: clinical trial Participants: 1,795 Evidence: high
Full summary, score breakdown and related studies → Original source
BackgroundDonanemab, a monoclonal antibody targeting amyloid-β (Aβ) plaques, has shown the ability to reduce cerebral amyloid burden in early Alzheimer's disease (AD). 2 key findings →
Design: systematic review Participants: 2,054 Evidence: high
Full summary, score breakdown and related studies → Original source
The primary study randomized 272 participants (mean [SD] age, 75.2 [5.5] years; 145 female participants [53.3%]). 3 key findings →
Design: clinical trial Participants: 272 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
No evidence of efficacy of 2 mg or 8 mg RSG XR monotherapy in cognition or global function was detected in the APOE-ε4-negative or other analysis populations. 2 key findings →
Design: open-label trial Participants: 693 Evidence: high
Full summary, score breakdown and related studies → Original source
The amyloid cascade model of the pathogenesis of Alzheimer disease (AD) is well supported in observational studies. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
PurposeTelephone disclosure of genetic test results can improve access to services. 4 key findings →
Participants: 257 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We sent invitations to 91,433 households; 5542 (6.1%) responded, 2120 completed the Baseline Survey (78.5% online; 21.5% via computer-assisted telephone interview), and 2087 were deemed eligible, yielding a response rate of 2.3%. 2 key findings →
Design: randomized controlled trial Participants: 374 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Among the 158 participants who accurately recalled their Alzheimer disease risk assessment 6 weeks after risk disclosure, 75 (47.5%) believed their Alzheimer disease risk was more than 5% points different from the Alzheimer disease risk estimate they were given. 2 key findings →
Design: randomized controlled trial Participants: 158 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
APOE -ε4 allele[s] is a risk factor for Alzheimer's disease (AD) and Amyloid-Related Imaging Abnormalities (ARIA) in anti-amyloid beta therapy, and is also associated with cerebrovascular risk factors such as hyperlipidemia or atherosclerosis. 4 key findings →
Participants: 6,313 Evidence: high
Full summary, score breakdown and related studies → Original source
ARIA-E incidence was 2.0% in non-carriers and 6.2% in εε4/εε4 homozygotes (εε4/εε4-versus-non-carrier OR 3.25, versus 8.49 in Clarity AD and 8.32 in Japan post-marketing surveillance). 4 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
We suggest that 6 months of dietary n-3 FA supplementation affected expression of genes that might influence inflammatory processes and could be of significance for AD. 3 key findings →
Participants: 16 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Disclosure of pleiotropic information did not increase anxiety or depression and may have decreased distress among persons at increased risk for 2 conditions. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Advances in genetic research have provided a basis for susceptibility testing for Alzheimer disease (AD). 2 key findings →
Design: randomized controlled trial Participants: 160 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
A condensed protocol for communicating genetic risk for Alzheimer disease achieved similar educational results as an extended protocol in this study. 3 key findings →
Participants: 280 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Higher baseline PP was significantly associated with increased Aβ (β = 0.078; p = 0.001), inferior temporal tau (β = 0.110; p = 0.032), and meta-temporal tau deposition (β = 0.116; p = 0.022). 4 key findings →
Design: cohort study Participants: 1,690 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Higher plasma carotenoid concentrations were associated with slower cognitive decline in APOE ε4 carriers, potentially mitigating genetic risk. 3 key findings →
Design: randomized controlled trial Participants: 442 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
At 6 mo, the n-3 FA group displayed marked increases in DHA and EPA plasma concentrations (2.6- and 3.5-fold), as well as decreased methylation in 2 out of 4 CpG sites ( P r = -0.25, P = 0.045; and r = -0.26, P = 0.041, respectively), but not to changes in plasma DHA concentration, and were not related to apolipoprotein E-4 allele frequency. 4 key findings →
Participants: 63 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Donepezil treatment slows the progression of hippocampal atrophy, suggesting a neuroprotective effect of donepezil in Alzheimer's disease. 2 key findings →
Design: cohort study Participants: 54 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Phenotypic personality dimensions, primarily neuroticism and extraversion, moderate the relationship between APOE [Latin Small Letter Open E]-4 genotype and cognitive outcomes among older adults. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The Risk Evaluation and Education for Alzheimer Disease study provides an instructive example of a process to develop risk assessment protocols that are sensitive to the implications of genetic testing for multiple ethnic groups with differing levels of risk. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
ApoE4 levels ascertained by the e4Quant test exhibited clear genotype-dependent stratification. 2 key findings →
Participants: 160 Evidence: low
Full summary, score breakdown and related studies → Original source
Defining the primary cognitive endpoint is a major decision for Alzheimer's disease preventive trials. 1 key finding →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Of 102 607 individuals in the study, 56 559 (55%) were women (median age, 58 years [IQR, 47-67 years]). 5 key findings →
Participants: 607 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 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 →