27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Midlife and late-life risk factors contributed to 22.7% and 16.5% of total dementia cases, respectively. 5 key findings →
Design: meta-analysis Participants: 37,931 Evidence: high
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Two regions achieved genome-wide significance with TDP-43: apolipoprotein E (APOE) and TMEM106B. Three loci reached genome-wide significance with HS: APOE, TMEM106B, and granulin precursor (GRN). 5 key findings →
Design: meta-analysis Participants: 9,509 Evidence: high
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The overall adherence rate to MI was 84.7%. 5 key findings →
Design: randomized controlled trial Evidence: high
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Donanemab treatment significantly slowed clinical progression at 76w and had a safety profile consistent with earlier studies. 5 key findings →
Participants: 1,182 Evidence: high
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While sex differences were not apparent at asymptomatic stages, females showed more rapid declines across all outcomes in symptomatic stages compared to males. 5 key findings →
Design: longitudinal study Participants: 337 Evidence: moderate
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Three progression clusters emerged in both cohorts: stable cognition, slow decline, and rapid decline-each including cases initially classified as CN or MCI. 5 key findings →
Design: longitudinal study Participants: 186 Evidence: moderate
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One hundred forty-nine carers enrolled in the study. 5 key findings →
Design: randomized controlled trial Participants: 149 Evidence: high
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The intervention group showed less discomfort (-1.06; 95% confidence interval [CI] = -1.88 to -0.23) and fewer sentinel events (-0.40; 95% CI = -0.64 to -0.16), specifically pneumonia (-0.08; 95% CI = -0.14, -0.02). 5 key findings →
Design: randomized controlled trial Participants: 116 Evidence: high
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NULISA plasma biomarkers revealed disease-specific protein patterns. 5 key findings →
Design: systematic review Participants: 194 Evidence: high
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Age- and education-adjusted hazard ratios (HRs) for ADRD increased as neighborhood disadvantage increased, to 1.42 (95% confidence interval [CI] 1.06-1.91) in the most disadvantaged quintile compared to the least disadvantaged quintile, with a significant linear trend (p = 0.012). 5 key findings →
Design: longitudinal study Participants: 10,915 Evidence: moderate
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WMHs in the frontoparietal and anterior periventricular region were associated with blood pressure traits, WMH genetic risk score (GRS), baseline and decline in general cognitive performance, incident all-cause dementia, and ischemic stroke. 5 key findings →
Design: longitudinal study Participants: 2,878 Evidence: moderate
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Females had higher rates of positive amyloid PET visual reads (63% vs. 59%, P < 0.001) and higher Centiloids (CLs; median 48.7 vs. 36.8, p < 0.001). 5 key findings →
Participants: 10,361 Evidence: moderate
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At baseline, Aβ+ participants showed higher CP FWf, increased white matter hyperintensity (WMH) volume, and decreased diffusion tensor image analysis along the perivascular space (DTI-ALPS). 5 key findings →
Design: cohort study Participants: 216 Evidence: moderate
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The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of developing criteria for the symptomatic predementia phase of Alzheimer's disease (AD), referred to in this article as mild cognitive impairment due to AD. 5 key findings →
Evidence: low
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Per 1-m/s increase in ePWV was associated with an adjusted hazard ratio (HR) (95% confidence interval [CI]) of 1.51(1.30-1.75) for dementia and 1.58(1.33-1.89) for Alzheimer's disease (AD), and with an MMSE score decline (adjusted β-coefficient = -0.36; 95% CI = -0.52 to -0.21). 5 key findings →
Design: longitudinal study Participants: 1,857 Evidence: moderate
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In multi-adjusted models, higher adherence to the EAT-Lancet diet was associated with higher total mean cortical thickness, and thicker cortex in Alzheimer's disease-signature regions, while a higher adherence to the MeDi was associated with better cognitive performance. 5 key findings →
Design: cohort study Participants: 615 Evidence: moderate
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There is increasing evidence that subjective cognitive decline (SCD) in individuals with unimpaired performance on cognitive tests may represent the first symptomatic manifestation of Alzheimer's disease (AD). 5 key findings →
Evidence: low
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Blood-based markers (BBMs) have recently shown promise to revolutionize the diagnostic and prognostic work-up of Alzheimer's disease (AD), as well as to improve the design of interventional trials.
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Non-specific codes were most common. Alzheimer's and vascular dementia codes showed high regional variability. 5 key findings →
Design: cohort study Participants: 2,016 Evidence: moderate
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Two hundred eighty dyads were enrolled. Caregivers during the intervention period reported lower levels of RSS of 0.7 points (standard deviation [SD]: 0.8) compared to the caregivers in the control period. 5 key findings →
Design: randomized controlled trial Evidence: high
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In addition to outperforming existing plasma biomarkers, the dSST predicted mid-life dementia risk over a 20-year follow-up across two independent cohorts with different ethnic backgrounds (areas under the curve [AUCs]: dSST 0.68-0.70, dSST+age 0.75-0.81). 4 key findings →
Design: longitudinal study Participants: 11,277 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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In 2006, the worldwide prevalence of Alzheimer's disease was 26.6 million. 5 key findings →
Participants: 85 Evidence: low
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During the past decade, a conceptual shift occurred in the field of Alzheimer's disease (AD) considering the disease as a continuum.
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Disclosure (N = 194) and non-disclosure (N = 180) groups did not differ on IGT-AD (mean disclosure-non-disclosure difference [MD] at 6 weeks: -1.5, p = 0.14; 9 months: -1.2, p = 0.35; 15 months: -2.0, p = 0.07), IES-R (MD at 6 weeks: 0.00, p = 0.98; 9 months: 0.01, p = 0.84; 15 months: 0.03, p = 0.64), or change in secondary outcomes. 4 key findings →
Design: randomized controlled trial Participants: 194 Evidence: high
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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →