The human metabolome reflects complex metabolic states affected by genetic and environmental factors. 5 key findings →
Participants: 23,000 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
The human metabolome reflects complex metabolic states affected by genetic and environmental factors. 5 key findings →
Participants: 23,000 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Full summary, score breakdown and related studies → Original source Free full text
Previously derived polygenic risk scores (PRSs) for Alzheimer's disease (AD) perform inconsistently across diverse ancestries. 3 key findings →
Design: cohort Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Identifying individuals at risk for developing Alzheimer disease (AD) is of utmost importance. 5 key findings →
Evidence: low
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Ninety-nine new cases of dementia (including 71 of Alzheimer disease) occurred during the follow-up. 4 key findings →
Evidence: low
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Recently, it has become clear that head trauma can lead to a progressive neurodegeneration known as chronic traumatic encephalopathy. 1 key finding →
Design: longitudinal study Evidence: moderate
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Artificially sweetened soft drink consumption was associated with a higher risk of stroke and dementia. 5 key findings →
Participants: 2,888 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is the most common cause of dementia worldwide, with the prevalence continuing to grow in part because of the aging world population. 1 key finding →
Evidence: low
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Systemic inflammation is associated with ischemia and Alzheimer disease (AD). 3 key findings →
Design: cross-sectional Evidence: low
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Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are devastating neurodegenerative disorders with clinical, genetic, and neuropathological overlap. 2 key findings →
Evidence: low
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Understanding normal brain aging and developing methods to maintain or improve cognition in older adults are major goals of fundamental and translational neuroscience. 3 key findings →
Evidence: low
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Mutations in APP, PSEN1, and PSEN2 lead to early-onset Alzheimer disease (EOAD) but account for only approximately 11% of EOAD overall, leaving most of the genetic risk for the most severe form of Alzheimer disease unexplained. 4 key findings →
Design: case-control study Evidence: moderate
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Four subtypes emerged: (1) dysnomic (n = 153), (2) dysexecutive (n = 102), (3) amnestic (n = 288), and (4) cluster-derived normal (n = 282) who performed within normal limits on cognitive testing. 4 key findings →
Participants: 153 Evidence: moderate
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Sleep disturbance is common in dementia, although it is unclear whether differences in sleep architecture precede dementia onset. 4 key findings →
Evidence: low
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The American Heart Association developed the ideal cardiovascular health (CVH) index as a simple tool to promote CVH; yet, its association with brain atrophy and dementia remains unexamined. 4 key findings →
Participants: 2,750 Evidence: moderate
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We categorized CVH on the basis of the American Heart Association Ideal CVH Index and genetic risk through a genetic risk score (GRS) of common genetic variants and the APOE ε4 genotype in 1,211 Framingham Heart Study (FHS) offspring cohort participants. 4 key findings →
Evidence: moderate
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Perivascular spaces (PVS) visible on MRI scans may represent key aspects in the pathophysiology of stroke and dementia, including cerebral small vessel disease and glymphatic dysfunction. 4 key findings →
Evidence: moderate
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In each cohort, achieving just 10-21.4 min/day moderate-to-vigorous PA related to better executive function ( P P = .02). 3 key findings →
Design: cross-sectional Participants: 1,861 Evidence: moderate
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This cohort study compares the risk of incident all-cause dementia among people with hearing loss who use vs do not use hearing aids. 1 key finding →
Design: cohort study Evidence: moderate
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We found no significant difference in dementia incidence over a 20‐year follow‐up period compared with matched TIA‐free controls. 3 key findings →
Design: cohort study Participants: 297 Evidence: high
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Of 10 974 participants (60.0% female, mean [SD] age: 73.2 [6.8] years), 2445 developed incident all-cause dementia over 116 067 person-years of follow-up. 5 key findings →
Participants: 974 Evidence: moderate
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White matter hyperintensities predict an increased risk of stroke, dementia, and death.
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The number of people with clinical AD will increase as the "baby boom" generation reaches older ages, exerting a strong upward influence on disease burden.
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Despite differences in prevalence of APOE-ε4, its association with dementia risk was similar across Chinese, Japanese, Filipino, and non-Latino White participants. 2 key findings →
Design: cohort Participants: 46,325 Evidence: moderate
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Similar to findings in adult mutation carriers, in the later preclinical and clinical stages of ADAD, mutation-carrying children were distinguished from control individuals by significantly higher plasma Aβ1-42 levels (mean [SD]: carriers, 18.8 [5.1] pg/mL and noncarriers, 13.1 [3.2] pg/mL; P Conclusions and relevance Children at genetic risk for ADAD have functional and structural brain changes and abnormal levels of plasma Aβ1-42. 2 key findings →
Design: cross-sectional 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →