30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among 5390 participants (mean [SD] age, 76.9 [4.8] years; 2915 women [54.1%]), there were 2655 individuals (49.3%) with less than 12 years of education. 5 key findings →
Design: case-control study Participants: 1,078 Evidence: moderate
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The pooled sample comprised 4657 participants (30% women) aged ≥ 60 years (mean age was 74 years at sleep assessment). 5 key findings →
Design: cohort study Participants: 2,374 Evidence: moderate
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One million nine hundred twenty-five thousand, five hundred sixty-three individuals were included across the four databases with a median follow-up ranging from 5.6 to 8.4 years. 4 key findings →
Design: meta-analysis Evidence: high
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AS01-adjuvanted shingles (herpes zoster) vaccination is associated with a lower risk of dementia, but the underlying mechanisms are unclear. 3 key findings →
Design: cohort study Participants: 436,788 Evidence: moderate
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Among 228 392 participants from UKB (n = 137 374; mean [SD] age at baseline, 62.5 [4.1] years; 53.8% female) and AOU (n = 91 018; mean [SD] age at baseline, 66.9 [7.8] years; 57.1% female), those with a history of a clinical exposure at baseline had higher dementia incidence rates compared with those without such history. 5 key findings →
Design: cohort study Participants: 137 Evidence: moderate
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In the prospective GLORIA-AF registry of AF patients, the presence of clinical complexity was associated with lower odds of being prescribed with OAC (odds ratio [OR] 0.50, 95% confidence interval [CI] 0.44–0.57), higher OAC discontinuation, and with a higher risk of adverse events (hazard ratio [HR] 1.63, 95% CI 1.43–1.86).[ 4 ] Indeed, “high clinical complexity” patients defined using latent class analysis constituted 6.6% of AF patients, and was associated with higher hazards of experiencing the primary composite outcome of all-cause death and major adverse cardiovascular events (HR 1.47, 95% 1.24–1.75).[ 5 ] Comorbidities and polypharmacy have an important influence on decision-making, by conditioning either lack of prescription of OAC in patients at risk or inappropriate dosing.[ 6 ] [ 7 ] [ 8 ] Recognizing that AF management is more than simply OAC alone, and requires a holistic and integrated care approach, contemporary guidelines globally on AF management have promoted this concept, based on the Atrial fibrillation Better Care (ABC) pathway, emphasizing Anticoagulation, Better symptom management with rate or rhythm control, and Comorbidity/lifestyle management.[ 9 ] [ 10 ] [ 11 ] The ABC pathway is well supported by clinical trial and real-world evidence,[ 11 ] whereby adherence to the ABC pathway is associated with a reduction in all-cause and cardiovascular mortality, stroke, and bleeding.[ 12 ] [ 13 ] Despite this, adherence to ABC-based management remains low, whereby a meta-analysis of 14 studies revealed that only 21% (95% CI 13–34%) of AF patients were managed in accordance with the ABC pathway.[ 12 ] This perhaps highlights a critical gap in the implementation of comprehensive evidence-based care strategies. 2 key findings →
Design: meta-analysis Evidence: high
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A total of 162 studies were included, with 88 (54.3%) exploring potential risk factors and 74 (45.7%) examining specific risk factors. 5 key findings →
Design: case-control study Participants: 162 Evidence: moderate
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Of 733 participants (mean age 82.5 ± 2.9 years), 164 (22.4%) developed MCI and 93 (12.7%) developed dementia by the follow-up visit. 5 key findings →
Design: longitudinal study Participants: 321 Evidence: moderate
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MarkVCID2 enrolled 1883 individuals age 73.4 ± 7.5 years, 65.0% female, 24.2% Hispanic, and 27.1% non-Hispanic Black. 5 key findings →
Design: longitudinal study Participants: 1,883 Evidence: moderate
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Benefit continued to accrue with ongoing lecanemab treatment through 36 months. 5 key findings →
Design: phase-3-trial Evidence: early
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Studies evaluating the diagnostic test accuracy of plasma phosphorylated tau (p-tau) and amyloid beta (Aβ) tests (p-tau217, %p-tau217, p-tau181, p-tau231, and Aβ42/Aβ40) compared to reference standard tests (cerebrospinal fluid [CSF] AD biomarkers, amyloid positron emission tomography [PET], or neuropathology) in individuals with cognitive impairment (mild cognitive impairment or dementia) in specialized care settings were included. 4 key findings →
Design: meta-analysis Evidence: moderate
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Cerebrospinal fluid (CSF) α-synuclein (α-syn) seed amplification assays (SAAs) can detect Lewy body pathology (LBP) with high accuracy but are invasive and costly. 2 key findings →
Design: cohort Participants: 1,567 Evidence: early
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The apolipoprotein E (APOE) gene is the best established genetic risk factor for Alzheimer's disease in later life, with the ε4 allele conferring higher risk. 5 key findings →
Design: cohort Participants: 9,496 Evidence: moderate
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Of 18 293 participants included in the parent study, scan images were available for 10 774 (59%), of which Centiloids were successfully calculated for 10 361 (96%). 1 key finding →
Design: cross-sectional Participants: 294 Evidence: low
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These findings suggest that PA may help delay cognitive decline by modulating neurodegeneration and AD-specific tau pathologies. 4 key findings →
Design: cross-sectional Participants: 1,144 Evidence: moderate
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Obicetrapib significantly slowed AD biomarker progression over 12 months in participants with ASCVD, with the greatest effects in ApoE4 carriers. 5 key findings →
Design: clinical trial Evidence: high
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The sample included 3 329 977 beneficiaries (2 126 290 [63.9%] female, 33 887 [1.0%] Asian, 354 771 [10.7%] Black, 61 515 [1.8%] Hispanic, 2 831 391 [85.0%] White, and 891 815 [26.8%] dual eligible for Medicaid). 5 key findings →
Design: cohort study Evidence: moderate
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A total of 807 K-ROAD participants (median age 72.0 years, 58.7% female) and 230 ADNI participants (median age 70.9 years, 49.1% female) were analyzed. 5 key findings →
Design: cohort study Participants: 807 Evidence: moderate
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Using the Swedish BioFINDER-2 cohort [n = 1702, 50.7% male, mean (standard deviation) age 68.4 (12.2) years], we compared the associations between tau/Aβ-PET load and fluid biomarkers alone versus biomarkers in a ratio with a reference protein (Aβ40 or np-tau) in univariate linear regression models. 5 key findings →
Design: longitudinal study Participants: 1,702 Evidence: moderate
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In a total of 602 autopsy cases (median [IQR] age at death, 78 [71-85] years; 328 male [54.5%] and 274 female [45.5%]), higher PM2.5 exposure prior to death was associated with increased odds of more severe Alzheimer disease neuropathologic change (ADNC) (odds ratio, 1.19; 95% CI, 1.11-1.28). 5 key findings →
Design: cohort study Participants: 602 Evidence: moderate
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Varicella-zoster virus (VZV) is a neurotropic virus that establishes lifelong latency in humans. 4 key findings →
Design: longitudinal study Evidence: moderate
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Among 2946 participants (mean [SD] age, 74.9 [4.6] years; 1751 [59.4] female; 637 Black [21.6%] and 2309 White [78.4%] individuals), 1947 participants (66.1%) had audiometric hearing loss, and 1097 (37.2%) had self-reported hearing loss. 5 key findings →
Design: cohort study Participants: 2,946 Evidence: moderate
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The study population consisted of 27 172 adults, including 4256 adults (14.0%) residing in rural areas, 14 741 (54.8%) in small or medium metropolitan areas, and 8175 (31.2%) in urban areas. 5 key findings →
Design: cross-sectional Participants: 172 Evidence: low
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The study sample included 1,375 participants free of dementia and stroke at baseline (mean age 68 ± 6y, 54 % females). 5 key findings →
Design: cohort study Participants: 1,375 Evidence: moderate
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Distinct associations between different traffic noise exposures and incident dementia subtypes were found in this large UK prospective cohort study. 3 key findings →
Design: cohort study Participants: 502,416 Evidence: moderate
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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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events