27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
It was not possible to demonstrate significant differences on the co-primary clinical endpoints (ADAS-cog 11 and ADCS-ADL 23 ) at 52 weeks due to symptomatic activity in the control arm. 5 key findings →
Design: phase-3-trial Participants: 598 Evidence: null result
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Over a mean follow-up of 8.4 years (range, Conclusions and relevance This cohort study of older adults found that adherence to a dietary pattern with lower inflammatory potential was associated with lower dementia risk among individuals with AD pathology and broader neurobiological risk. 3 key findings →
Design: cohort Participants: 1,865 Evidence: early
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APOE ε4 carriers have increased Alzheimer's disease risk and altered omega-3 metabolism. 5 key findings →
Design: phase-2-trial Participants: 365 Evidence: null result
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The effects on depression and other outcomes were consistent with those observed for in-person programs, suggesting the viability of well-designed automated intervention. 2 key findings →
Design: RCT Participants: 274 Evidence: moderate
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Longer follow-up and testing across diverse LEP communities are needed to assess diagnosis, treatment initiation, and caregiver trajectories. 1 key finding →
Design: RCT Participants: 287 Evidence: moderate
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We found that ApoE4 did not facilitate amyloid-PET-associated ptau increases, suggesting that amyloid-related ptau secretion is not altered by ApoE4 carriage. 4 key findings →
Design: cohort Participants: 401 Evidence: moderate
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This study included 10 333 FHS 5 key findings →
Design: cohort study Participants: 886 Evidence: moderate
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Our sample included 11,105 patients (median age 77, 51% female), with 2299 in the hallway group and 8806 in the non-hallway group. 5 key findings →
Design: retrospective cohort Participants: 11,105 Evidence: moderate
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Of 689 participants, CI was associated with delirium (adjusted odds ratio [aOR]: 3.64, 95% CI: 1.31, 9.49, P-value = 0.009), 90-day complications (aOR: 2.26, 95% CI: 1.14, 4.28, P-value = 0.015), and 90-day composite adverse outcomes (aOR: 2.03, 95% CI: 1.03, 3.81, P-value = 0.033). 5 key findings →
Design: cohort study Participants: 689 Evidence: moderate
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First, based on pooled results of RCTs, the melatonin agonists melatonin and ramelteon were not found to reduce delirium incidence (RR 0.94, 95% CI 0.72–1.22, k = 16 studies; RR 0.63, 95% CI 0.39–1.03, k = 8, respectively). 5 key findings →
Design: systematic review Participants: 203 Evidence: high
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A total of 42 342 participants from the pooled cohorts were included (mean [SD] age, 61.3 [9.8] years; 55.0% female). 5 key findings →
Design: cohort study Participants: 342 Evidence: moderate
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Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status. 5 key findings →
Design: cohort Participants: 8,582 Evidence: high
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One hundred sixteen participants consented and 93 (46 waitlist control, 47 intervention) were included in the analyses. 3 key findings →
Design: RCT Participants: 93 Evidence: null result
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Peer support interventions suggest beneficial short-term effects on specific caregiver outcomes but lack long-term sustainability. 3 key findings →
Design: meta-analysis Participants: 1,680 Evidence: moderate
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These results suggest that all adults with Down syndrome should be screened for Alzheimer's disease pathology starting shortly before age 40 years and considered for clinical trials. 1 key finding →
Design: longitudinal study Participants: 328 Evidence: moderate
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The analytic sample included 1 054 926 beneficiaries, including 219 942 (mean [SD] age, 75.3 [6.3] years; 54.6% female) who developed new complex conditions in 2019 and 834 984 (mean [SD] age, 73.8 [5.6] years; 56.7% female) who did not develop a new complex condition in 2019. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among 2157 older adults without dementia (mean [SD] age 71.2 [9.2] years; 1337 female [62.0%]), 1680 participants had longitudinal cognition data and 569 participants (26.4%) had APOE34/44 genotypes. 5 key findings →
Design: cohort study Participants: 1,680 Evidence: moderate
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In this study's cohort of 155 individuals with SETRS (mean [SD] age, 59.3 [10.3] years; 56 female participants [36.1%]), 153 of 155 (98.7%) scored below the cutoff of 26 for mild cognitive impairment, and 73 of 155 (47.1%) scored below the cutoff of 10 for severe dementia (mean [SD] MoCA score, 9.8 [6.4]). 5 key findings →
Design: cohort study Participants: 155 Evidence: moderate
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Accurate diagnosis of dementia with Lewy bodies (DLB) remains challenging, with misdiagnosis potentially leading to harmful treatment decisions. 3 key findings →
Participants: 740 Evidence: moderate
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BackgroundAlzheimer's disease (AD) accounts for the majority of dementia-related disorders among aging populations. 2 key findings →
Design: systematic review Evidence: high
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Alzheimer's disease (AD) is a major cause of dementia and cognitive decline. 3 key findings →
Design: longitudinal study Evidence: moderate
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The telmisartan group had the lowest risk of all dementias (telmisartan vs NT-ARB: hazard ratio [HR]: 0.78; 95% confidence interval [CI]: 0.60 to 1.01; telmisartan vs angiotensin-converting enzyme inhibitor: HR: 0.67; 95% CI: 0.48 to 0.94). 5 key findings →
Design: cohort study Participants: 39,665 Evidence: moderate
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Overall, the available evidence suggests that natural compounds confer multitarget neuroprotective effects that directly engage with key pathological mechanisms underlying AD. 4 key findings →
Design: systematic review Participants: 41 Evidence: high
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False-positive (FP) plasma results may lead to overtreatment and false-negative (FN) results to missed or delayed disease-modifying therapies. 5 key findings →
Participants: 706 Evidence: low
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Greater multimorbidity burden was associated with worse cognition and biomarkers of AD (PET amyloid standardized uptake value ratios and positivity, p-tau181, and p-tau217), neurodegeneration (neurofilament light, total tau, cortical thickness, and hippocampal volume), and SVD (white matter hyperintensity volume and presence of lacune and cerebral microbleeds). 3 key findings →
Participants: 3,808 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 →