28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The advent of anti-amyloid monoclonal antibody (mAb) therapies represents a paradigm shift in the treatment of Alzheimer's disease (AD), from symptomatic relief to disease modification. 5 key findings →
Design: randomized controlled trial Evidence: high
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Most patients with svMCI do not exhibit substantial amyloid burden, and CVD does not increase β-amyloid burden as measured by amyloid imaging. 5 key findings →
Design: cross-sectional Participants: 95 Evidence: low
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Although air pollution is well known to be harmful to the lung and airways, it can also damage most other organ systems of the body. 4 key findings →
Evidence: low
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The data of 508,107 individuals were analyzed (mean [standard deviation] age, 67.6 [10.7] years; 66.8% women and 33.2% men), and 39,318 developed Alzheimer's disease (22,572 controls and 16,746 using aspirin). 5 key findings →
Design: cohort study Participants: 508,107 Evidence: moderate
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Tau PET imaging with (18)F-AV-1451 could serve as an in vivo biomarker for the evaluation of AD-related tau pathology and monitoring disease progression. 2 key findings →
Participants: 20 Evidence: low
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Our data suggest that structural MRI can be used to identify biologically and clinically meaningful subtypes of AD. 3 key findings →
Evidence: low
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Over a median follow-up of 13.5 years, 1453 dementia cases were identified. 5 key findings →
Participants: 131,209 Evidence: moderate
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Our findings suggest that poor chewing ability is associated with cognitive impairment or dementia in the elderly living in rural area. 4 key findings →
Design: cross-sectional Participants: 295 Evidence: low
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We conducted a retrospective cohort study using the National Health Insurance Database in South Korea. 5 key findings →
Design: cohort study Evidence: moderate
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Over 13.45 years, 992 all-cause dementia cases were recorded. 5 key findings →
Design: cohort study Participants: 118,963 Evidence: moderate
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Alzheimer disease (AD) is associated with an increase in the brain of the 18-kDa translocator protein (TSPO), which is overexpressed in activated microglia and reactive astrocytes. 4 key findings →
Evidence: low
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= 0.041). Socioeconomic status and residential area are associated with long-term survival in patients with EOD. 2 key findings →
Design: cohort study Participants: 3,825 Evidence: moderate
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The prominent prognostic role of carotid plaques in Aβ-negative MCI underscores the vascular contributions to non-amyloid cognitive decline and highlights the importance of evaluating both AD-related and vascular mechanisms in prodromal dementia. 1 key finding →
Design: longitudinal study Participants: 58 Evidence: moderate
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We assessed 452,718 patients (mean age: 67.16 years). 3 key findings →
Design: cohort study Participants: 452,718 Evidence: moderate
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This study developed machine learning models to predict Aβ positivity in Alzheimer’s disease by integrating early-phase 18 F-Florbetaben PET and clinical data to improve diagnostic accuracy. 2 key findings →
Participants: 176 Evidence: low
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There was an age-related increase in both 18 F-AV-1451 binding in the basal ganglia and R 2 * values in the putamen in both the controls and the Alzheimer disease/mild cognitive impairment patients. 18 F-AV-1451 binding in the basal ganglia increased with R 2 * values. 3 key findings →
Participants: 61 Evidence: low
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Hypertension is the leading modifiable risk factor for atrial fibrillation (AF) and is estimated to be present in >70% of AF patients. 1 key finding →
Evidence: low
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High LDL-C (≥160 mg/dL) increased AD risk across all groups {hazard ratio (HR): 1.23 [95% confidence interval (CI): 1.10-1.38],p<0.001;HR: 1.45 (95% CI: 1.08-1.93),p=0.013;HR: 1.25 (95% CI: 1.10-1.42),p<0.001, respectively}, whereas low LDL-C (<70 mg/dL) showed higher VD risk in those not taking cholesterol-lowering medication [HR: 3.02 (95% CI: 1.73-5.27),p<0.001].Low HDL-C (≤40 mg/dL) was associated with increased AD and VD risk in non-users. 2 key findings →
Design: cohort study Evidence: moderate
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These results suggest that 4-O-methylhonokiol inhibits LPS-induced amyloidogenesis via anti-inflammatory mechanisms. 3 key findings →
Evidence: low
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Growing dementia prevalence underscores the need for efficient screening methods, but lengthy digital assessments often cause fatigue among older adults. 1 key finding →
Participants: 297 Evidence: low
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Our findings imply that the current version of the Boston criteria may not be sufficient enough to remove non-CAA cases from a cognitively impaired population, especially in the absence of cSS. 4 key findings →
Participants: 27 Evidence: low
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Cortical thickness from MRI helped predict conversion from mild cognitive impairment to dementia in Parkinson disease at an individual level, with improved performance when integrated with clinical variables. © RSNA, 2021 Online supplemental material is available for this article. 2 key findings →
Participants: 75 Evidence: low
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Most individuals with Down syndrome show early onset of Alzheimer disease (AD), resulting from the extra copy of chromosome 21. 4 key findings →
Evidence: low
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Plasma p-tau217-based biomarkers showed excellent detecting performance for early amyloid (Thal I-II; area under the curve values > 0.96) and intermediate tau (Braak III-IV; area under the curve values > 0.92). 5 key findings →
Participants: 237 Evidence: low
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Dementia was significantly associated with caregiver burden related to emotional difficulty (odds ratio [OR] = 2.04; 95% confidence interval [CI], 1.34-3.09) and physical difficulty (OR = 1.67, 95% CI, 1.01-2.78), but not financial difficulty. 3 key findings →
Participants: 1,419 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →