Brain structure in later life reflects both influences of intrinsic aging and those of lifestyle, environment and disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Brain structure in later life reflects both influences of intrinsic aging and those of lifestyle, environment and disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A growing body of literature has suggested that obstructive sleep apnea (OSA) and habitual short sleep duration are linked to poor cognitive function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among 5757 participants (21.7% Black, 20.3% Latinx, 58.1% AORE), we found lower odds of amyloid positivity in Black (odds ratio [OR]: 0.72, 95% confidence interval [CI]: 0.62-0.83) and Latinx (OR: 0.78, 95% CI: 0.67-0.91) compared to AORE. 4 key findings →
Participants: 5,757 Evidence: moderate
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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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Of the 944 clinical cases, 13.0% were characterized as probable LATE (2.4% pure LATE and 10.6% LATE+AD) and 23.7% were characterized as probable AD without LATE. 5 key findings →
Participants: 944 Evidence: low
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CSF Aβ42/Aβ40 contributed most to identify Aβ-positivity, while continuous Aβ-PET load within the positive range was best predicted by plasma P-tau217. 1 key finding →
Participants: 1,053 Evidence: low
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EXT showed high cross-sectional reliability and longitudinal stability. 5 key findings →
Design: cross-sectional Evidence: moderate
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The advent of amyloid-β (Aβ) and tau PET imaging has revolutionized Alzheimer disease (AD) research, enabling in vivo detection of hallmark pathologies and transforming both diagnosis and therapeutic development. 5 key findings →
Evidence: low
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This paper introduces a novel convolutional neural network model with an attention mechanism to advance Alzheimer disease (AD) classification using Magnetic Resonance Imaging (MRI). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
< 0.001), with the automated approach more likely to classify a scan as tau negative and lower agreement between methods in more severe cases and AD clinical variants. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Traditional diagnostic methods for Alzheimer's disease often suffer from low accuracy and lengthy processing times, delaying crucial interventions and patient care. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 0.120). These findings suggest that DESH and high EI, often considered biomarkers for iNPH, may lack specificity and may be found in a subset of patients with PSP or LBD leading to unnecessary neurosurgery for iNPH. 1 key finding →
Participants: 190 Evidence: low
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< 0.035), consistent with a neurodegenerative pattern. 3 key findings →
Evidence: low
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16% of individuals were identified as tau-accumulators. 5 key findings →
Design: longitudinal study Participants: 29 Evidence: moderate
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These results provide clear evidence that CU older adults with both amyloid plaques and tau aggregates measured with PET will develop cognitive impairments if the disease is not stopped. 2 key findings →
Design: cohort study Evidence: moderate
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Alzheimer's disease is associated with pre-symptomatic changes in brain morphometry and accumulation of abnormal tau and amyloid-beta pathology. 4 key findings →
Design: cross-sectional Evidence: moderate
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Metabolomics has been associated with cognitive decline and dementia, but the relationship between metabolites and brain aging remains unclear. 4 key findings →
Participants: 17,770 Evidence: low
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Frontotemporal dementia (FTD) is a neurodegenerative disorder primarily affecting the frontal and temporal lobes, leading to significant impairments in executive function, social behavior, and emotional regulation. 3 key findings →
Design: cohort study Evidence: moderate
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Alzheimer's disease (AD) develops over a prolonged asymptomatic phase marked by silent pathology. 1 key finding →
Participants: 102 Evidence: low
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The mean age of the sample was 63 years (Q1, Q3, 56, 68); 56% were women. 5 key findings →
Participants: 15,180 Evidence: low
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BackgroundA novel neuroimaging signature of regional cortical thickness on brain MRI recently showed high potential for Alzheimer's disease and related dementias (ADRD) risk stratification in the community. 1 key finding →
Design: cross-sectional Participants: 3,249 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
After controlling for the level of cognitive impairment, we found a double dissociation between AD clinical phenotype and localization/magnitude of atrophy, characterized by predominant neocortical involvement in EOAD and more focal anterior medial temporal involvement in LOAD. 5 key findings →
Evidence: low
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Differentiation of Alzheimer disease dementia (ADD) and dementia with Lewy bodies (DLB) remains a challenge. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Pulse pressure, but not mean arterial pressure, significantly mediated the relationship between age and white matter hyperintensity load. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The plasma PlGF level was significantly elevated in patients with SIVD compared with CUCs, and showed a high accuracy with an area under the curve of 0.893. 5 key findings →
Participants: 102 Evidence: moderate
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.
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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% 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 →