Among 209,468 decedents, 95,594 were selected after matching. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among 209,468 decedents, 95,594 were selected after matching. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 2935 patients (50.4% women; mean age=72.2 years; 19.8% subjective cognitive impairment, 39.8% mild cognitive impairment, and 40.4% dementia), larger WMH volume within projection fibres (B=0.24, SE=0.10, p=0.013) was associated with greater apathy. 5 key findings →
Participants: 2,935 Evidence: low
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Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia with no specific treatment, of which molecular mechanisms remain poorly understood. 2 key findings →
Participants: 40,000 Evidence: low
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Our aim is to examine the interplay between cerebral small vessel disease (CSVD) pathology, Alzheimer’s disease (AD) related amyloid-β (Aβ) clearance, and cognition in general population. 2 key findings →
Design: cross-sectional Participants: 1,026 Evidence: moderate
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This study included 3540 participants with RVC data and 489 with WMH data (median [IQR] age: 73.2 [71.4-76.3] and 72.5 [71.2-75.4] years; female: 52.9% and 47.6%) over a median follow-up of 7.4 [IQR 5.5-8.5] and 3.8 [IQR 2.9-5.3] years, respectively. 5 key findings →
Design: cross-sectional Participants: 3,540 Evidence: moderate
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Out of 462,327 eligible participants, those with constipation were associated with higher incidence of three outcome diseases (1415/20,263 [7.0%]) than those without (18,848/442,064 [4.3%]), with adjusted hazard ratio (HR) being 1.35 [1.27-1.42]. 5 key findings →
Design: cohort study Evidence: moderate
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Hypertension, acute myocardial infarction, atrial fibrillation, diabetes, heart failure, ischemic heart disease, stroke, and arthritis additively accounted for 71.8% (95% confidence interval [CI]: 62.9%-79.1%) of ADRD incident cases based on LE-AAF. 5 key findings →
Design: longitudinal study Evidence: moderate
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This study evaluates the efficacy, safety, and economics of galantamine in the treatment of Alzheimer disease (AD) patients, and to provide evidence-based reference for optimizing drug selection, dosing strategies, and reimbursement policies in clinical practice. 5 key findings →
Design: systematic review Evidence: high
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Recent guidance from the National Alzheimer's Coordinating Center (NACC) recommends remuneration for all Alzheimer's disease (AD) research participants. 5 key findings →
Design: longitudinal study Participants: 29 Evidence: moderate
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This bibliometric analysis provides a comprehensive overview of research trends in immune-related cognitive impairment. 2 key findings →
Design: systematic review Participants: 3,737 Evidence: low
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Although pathogenic variants in PSEN1 leading to autosomal-dominant Alzheimer disease (ADAD) are highly penetrant, substantial interindividual variability in the rates of cognitive decline and biomarker change are observed in ADAD. 3 key findings →
Design: cross-sectional Evidence: moderate
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Our meta-analyses confirmed significantly lower CSF TAU levels in DLB and CSF SYUA levels in PDD, when compared to Alzheimer's disease. 4 key findings →
Design: systematic review Evidence: high
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This study summarizes the existing literature on TSPO expression in specific regions of the brain in patients with dementia, and also provides some preliminary evidence on the possible association between neuroinflammation and dementia. 5 key findings →
Design: meta-analysis Evidence: high
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Bile acids (BAs) may contribute to dementia by regulating neuroinflammation and influencing gut-brain axis signaling, especially in Alzheimer's disease (AD). 3 key findings →
Design: cross-sectional Evidence: moderate
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The incidence rate for AD was significantly higher among African-American and Caribbean Hispanic elderly individuals compared white individuals.
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Rates of hippocampal atrophy match both baseline cognitive status and the change in cognitive status over time in elderly persons who lie along the cognitive continuum from normal to MCI to AD.
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PiB and florbetapir retention ratios were strongly associated in the same individuals, and this relationship was consistent across several data analysis methods, despite scan-rescan intervals of more than a year.
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Apolipoprotein E (apoE) alleles determine the age-adjusted relative risk (epsilon4 > epsilon3) for Alzheimer's disease (AD).
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Among 455,306 UK Biobank participants, 37 carried one copy of the APOE Christchurch variant (allele frequency 0.004%). 4 key findings →
Design: cohort Participants: 455,306 Evidence: early
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Healthcare costs are already elevated in early subjective and objective cognitive impairment, driven by formal and informal care. 5 key findings →
Design: cross-sectional Evidence: moderate
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Recently, ~16% of participants in an anti-Aβ passive immunotherapy trial for mild-to-moderate Alzheimer disease (AD) had a negative baseline amyloid positron emission tomography (PET) scan. 1 key finding →
Evidence: low
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Amyloid imaging is currently introduced to the market for clinical use. 5 key findings →
Design: cross-sectional Evidence: moderate
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Infections have been associated with the incidence of Alzheimer disease and related dementias, but the mechanisms responsible for these associations remain unclear. 4 key findings →
Evidence: low
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After disclosure, 27 patients with amyloid-positive SCD+ (median [IQR] age, 70 [66-74] years; gender: 14 men [52%]; median [IQR] education: 15 [13 to 17] years, median [IQR] Mini-Mental State Examination [MMSE] score, 29 [28 to 30]) had higher median (IQR) IES-R total score (10 [2 to 14] vs 0 [0 to 2]; P Conclusions and relevance The disclosure of a positive amyloid-PET result to patients with SCD+ was associated with a bigger psychological change, yet such change did not reach the threshold for clinical concern. 5 key findings →
Participants: 27 Evidence: low
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Participants with higher total-tau and NfL at baseline had a higher risk of stroke and several stroke subtypes. 5 key findings →
Participants: 379 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 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 →