27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The study included 732 participants (median [IQR] age, 41 [34.0-48.0] years; 369 [50.4%] male; 64 [8.9%] Black or African American, 587 [81.3%] White, and 71 [9.8%] other races); 414 reported baseline FTS use and 318 did not. 5 key findings →
Design: cohort study Participants: 732 Evidence: moderate
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Sample 1 included 1656 participants (mean [range] age, 58.1 [29.7-85.6] years; 903 female [54.5%]), and sample 2 included 935 participants (mean [range] age, 67.6 [60.0-85.6] years; 518 female [55.4%]). 4 key findings →
Design: cohort study Participants: 1,656 Evidence: moderate
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A total of 450 111 participants were included in the study (mean [SD] age, 51.1 [9.8] years; 70.8% women) and followed up during a median (IQR) time of 14.9 (4.1) years. 5 key findings →
Design: cohort study Participants: 111 Evidence: moderate
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Of the 14 685 participants (7355 female [50%] and 7330 male [50%]; mean [SD] age, 73.8 [8.5] years) who met the inclusion criteria, 221 participants (1.5%) developed LOE during follow-up. 5 key findings →
Design: longitudinal study Participants: 713 Evidence: moderate
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Mean age ± SD was 83.4 ± 9.1 years. Most were female (72.0%), white (92.3%), non-Hispanic (84.6%), and lived in nursing homes (76.9%). 5 key findings →
Design: randomized controlled trial Participants: 147 Evidence: high
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Evidence regarding the clinical validity of blood biomarkers of Alzheimer's disease (AD) in the general population is limited. 3 key findings →
Evidence: moderate
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Blood-based biomarkers for Alzheimer's disease (AD) pathology have been investigated intensively as markers for AD-related neurodegeneration. 5 key findings →
Design: cohort study Participants: 158 Evidence: moderate
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Social isolation was significantly associated with reduced cognitive ability (pooled effect = -0.07, 95% CI = -0.08, -0.05), with consistently negative effects across memory, orientation, and executive ability. 4 key findings →
Design: meta-analysis Participants: 101,581 Evidence: high
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After a median follow-up time of 14.3 (7.9-20.0) years, dementia was recorded in 530 (1.2%) individuals with type 1 diabetes and 1,867 (0.9%) age-, sex-, and county-matched control individuals (mean baseline age 33.0 [14.0] years). 4 key findings →
Design: cohort study Participants: 43,440 Evidence: moderate
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Over a mean follow-up of 7.9 years, 694 incident dementia cases occurred. 5 key findings →
Design: cohort study Participants: 82,391 Evidence: moderate
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= 0.009). Significant differences in annualized changes in these FA and MD values were found depending on the presence or absence of type 2 diabetes and smoking. 4 key findings →
Design: longitudinal study Participants: 6,471 Evidence: moderate
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Based on positive/negative results on the different biomarkers, subjects were classified as 'AD-LB-' (n = 304), 'AD+LB-' (n = 335), 'AD+LB+' (n = 158) and 'AD-LB+' (n = 68). 5 key findings →
Design: longitudinal study Participants: 661 Evidence: moderate
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Among 2556 patients (mean age 79 ± 9 years; 56% women), delirium occurred in 957 (37%). 5 key findings →
Design: cohort study Participants: 2,556 Evidence: moderate
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Apolipoprotein E, type epsilon 4 allele (APOE epsilon 4), is associated with late-onset familial Alzheimer's disease (AD). 3 key findings →
Evidence: low
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Meta-analysis of the 2 family-based and the 5 case-control cohorts yielded a p value of 0.0029, while the overall summary estimate (using case-control data only) resulted in an odds ratio of 1.67 (95% confidence interval 0.95-2.92) for the association between the TREM2 R47H and increased AD risk. 3 key findings →
Design: meta-analysis Evidence: high
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In patients with Alzheimer's disease pathophysiological changes of the brain that initiate the onset of Alzheimer's disease include accumulation of amyloid-β plaques and phosphorylation of tau-tangles. 1 key finding →
Design: systematic review Participants: 1,962 Evidence: high
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These results suggest that AADvac1 tau immunotherapy can reduce plasma biomarkers of neurodegeneration and neuroinflammation. 4 key findings →
Design: post-hoc analysis Evidence: high
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Synapse loss in Alzheimer's disease (AD) correlates with cognitive decline. 4 key findings →
Evidence: low
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The online SiD decision aid increased preparation for decision making about firearm access in this sample of ADRD caregivers in the United States. 5 key findings →
Design: RCT Participants: 500 Evidence: moderate
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Music Interventions for Dementia and Depression in Elderly care was a large, multinational, cluster-randomised controlled trial with a 2 × 2 factorial design to examine the effects of group music therapy, recreational choir singing, or both compared with standard care. 2 key findings →
Design: RCT Participants: 1,021 Evidence: null result
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No significant difference between the three groups in ADAS-Cog was found at the primary endpoint at 15 months (CPR vs health advice, β= -0·04 [95% CI -0·34 to 0·26]; RFM vs health advice, β= -0·14 [-0·44 to 0·15]; CPR vs RFM, β=0·10 [-0·19 to 0·40]) nor at the 6-month and 12-month follow-ups. 1 key finding →
Design: RCT Participants: 456 Evidence: null result
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APOE shows a heterogeneous effect on ADRD risk in our Hispanics/Latinos sample, the largest to date. 4 key findings →
Design: case-control Participants: 12,221 Evidence: moderate
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Nonlinear dose-response relationship between exercise and cognitive improvement in Alzheimer's disease, with the optimal AE dose identified at 660 METs-min/week for enhancing cognitive function in AD. 3 key findings →
Design: meta-analysis Participants: 2,242 Evidence: early
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Our findings illuminate the potential benefits of ChEI treatment in DLB patients. 4 key findings →
Design: cohort Participants: 1,095 Evidence: moderate
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No benefits were demonstrated for secondary clinical end points. 3 key findings →
Design: phase-2-trial Participants: 327 Evidence: null result
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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 27,380 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 →