27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Data from 1,272,495 individuals, with the mean age at diagnosis ranging from 76.8 years (South Korea) to 82.9 years (Germany), show that the overall median length of survival following recorded diagnosis ranges from 2.4 years (New Zealand) to 7.9 years (South Korea). 2 key findings →
Design: cohort study Participants: 1,272,495 Evidence: moderate
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This cluster analysis of cortical thickness of the entire brain showed that AD dementia in the earlier stages can be categorized into various anatomical subtypes, with distinct clinical features. 5 key findings →
Participants: 52 Evidence: low
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In the present study, our automated classifier successfully classified FTD clinical subtypes with good to excellent accuracy. 1 key finding →
Participants: 143 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The discovery of TREM2 as a myeloid-specific Alzheimer's disease (AD) risk gene has accelerated research into the role of microglia in AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
During follow-up ranging from 1.0 to 22.9 years, 75 patients (29.88%) converted to AD. 5 key findings →
Design: longitudinal study Participants: 75 Evidence: moderate
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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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We previously developed a novel machine-learning-based brain age model that was sensitive to amyloid. 3 key findings →
Participants: 757 Evidence: low
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A total of 322 participants with p-tau217, GFAP, and NfL analyses were stratified into the EOAD or FTD group based on their diagnosis. 5 key findings →
Design: cohort study Participants: 245 Evidence: moderate
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This narrative review integrates longitudinal cohort studies, neuroimaging and biomarker research, and major clinical trials to examine how depression and cognitive decline interact across the dementia continuum. 3 key findings →
Design: cohort study Evidence: moderate
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SVaD without abnormal amyloid imaging was more common than expected. 4 key findings →
Participants: 45 Evidence: low
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The Seoul Neuropsychological Screening Battery (SNSB) is one of the standardized neuropsychological test batteries widely used in Korea. 4 key findings →
Participants: 43 Evidence: low
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Dementia risk was significantly higher in patients with epilepsy compared with that of controls (IRR: 3.65; 95% CI: 3.14-4.24), especially within the first 2 years post-diagnosis (aHR: 5.42; 95% CI: 4.30-6.83), peaking between 8 and 10 years (aHR: 8.25; 95% CI: 3.15-21.5). 5 key findings →
Design: cohort study Participants: 2,740 Evidence: moderate
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Oxidative stress is thought to play a role in the pathogenesis of Alzheimer's disease (AD) and increased oxidative DNA damage has been observed in brain tissue from AD patients. 3 key findings →
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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The membrane protein TREM2 (Triggering Receptor Expressed on Myeloid cells 2) regulates key microglial functions including phagocytosis and chemotaxis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
During a mean follow-up of 2.49 years (median, 1.99; standard deviation, 2.07; interquartile range, 2.66), dementia was significantly associated with increased stroke risk (aHR, 3.19; 95% confidence interval, 2.84-3.57). 5 key findings →
Design: cohort study Participants: 2,820 Evidence: moderate
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The study included 807 participants form K-ROAD (median age: 72.0 years, 58.7% female) and 230 from ADNI (median age: 70.9 years, 49.1% female). 5 key findings →
Design: cohort study Participants: 807 Evidence: moderate
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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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The Montreal Cognitive Assessment (MoCA) is a brief cognitive screening tool with high sensitivity for screening patients with mild cognitive impairment (MCI). 1 key finding →
Evidence: low
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We investigated the changes of sulcal shape (average mean curvature in folded regions and sulcal depth) in mild cognitive impairment (MCI) and Alzheimer's disease (AD) using quantitative surface-based methods in a large sample of magnetic resonance imaging data. 4 key findings →
Evidence: low
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The machine learning algorithm for NPTs has suggested potential use as a reference in differentiating cognitive impairment in the clinical setting. 1 key finding →
Evidence: low
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Alzheimer disease (AD) is characterized by amyloid-β plaques (A), tau tangles (T), and neurodegeneration (N), collectively defining the ATN framework. 4 key findings →
Design: longitudinal study Evidence: moderate
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Laboratory-specific reference values for cerebrospinal fluid (CSF) Alzheimer disease (AD) biomarkers are necessary. 4 key findings →
Participants: 71 Evidence: low
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Current evidence suggests a central role for autophagy in Alzheimer disease (AD), and dysfunction in the autophagic system may lead to amyloid-β (Aβ) accumulation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings establish IF as a potent modulator of synaptic resilience in VaD, acting through coordinated preservation of synaptic structure, inhibition of inflammatory synapse loss, and metabolic reprogramming. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →