Macrophage-mediated inflammation is critical in the pathogenesis of non-alcoholic steatohepatitis (NASH). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Macrophage-mediated inflammation is critical in the pathogenesis of non-alcoholic steatohepatitis (NASH). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The microglial receptors CD33 and TREM2 have been associated with risk for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a neurodegenerative disease that causes late-onset dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Sepsis is a leading cause of death in critical illness, and its pathophysiology varies depending on preexisting medical conditions. 4 key findings →
Evidence: moderate
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The four emerging CSF biomarkers were significantly elevated in the mutation carriers (n = 235) versus noncarriers (n = 145). 4 key findings →
Participants: 235 Evidence: low
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Two genetic variants in strong linkage disequilibrium (rs9536314 and rs9527025) in the Klotho (KL) gene, encoding a transmembrane protein, implicated in longevity and associated with brain resilience during normal aging, were recently shown to be associated with Alzheimer disease (AD) risk in cognitively normal participants who are APOE ε4 carriers. 4 key findings →
Participants: 5,541 Evidence: low
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Brain amyloid-beta (Aβ) plaques, a hallmark of the pathophysiology of Alzheimer's disease, have been associated with frailty. 4 key findings →
Participants: 477 Evidence: low
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It remains unknown whether the associations between protective lifestyles and sporadic dementia risk reported in observational studies also affect age at symptom onset (AAO) in autosomal dominant Alzheimer disease (ADAD) with predominant genetic influences. 4 key findings →
Design: longitudinal study Participants: 103 Evidence: moderate
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Alzheimer's disease (AD) pathology is defined by β-amyloid (Aβ) plaques and neurofibrillary tau, but Lewy bodies (LBs; 𝛼-synuclein aggregates) are a common co-pathology for which effective biomarkers are needed. 4 key findings →
Evidence: low
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Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. 4 key findings →
Evidence: low
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After adjusting for demographics, apolipoprotein E (APOE) ε4 status, cognition, and comorbidities, the highest tertile of REM latency was associated with higher Aβ burden (β = 0.08, 95% confidence interval [CI]: 0.03 to 0.13, p = 0.002), elevated p-tau181 (β = 0.19, 95% CI: 0.02 to 0.13, p = 0.002), and reduced BDNF levels (β = -0.47, 95% CI: -0.68 to -0.13, p = 0.013), compared to the lowest tertile. 5 key findings →
Participants: 128 Evidence: low
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Nuclear depletion and cytoplasmic aggregation of the RNA-binding protein TDP-43 are cellular hallmarks of amyotrophic lateral sclerosis (ALS). 1 key finding →
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
Full summary, score breakdown and related studies → Original source Free full text
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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Regional sex-related differences in tau PET burden may contribute to the disparities in AD prevalence between males and females. 4 key findings →
Design: cross-sectional Participants: 148 Evidence: moderate
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These results provide evidence that, in the absence of significant neurodegenerative processes, individuals who harbor AD neuropathology may remain cognitively unimpaired. 4 key findings →
Design: cross-sectional Participants: 79 Evidence: low
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Neurotoxic amyloid beta peptide (Abeta) accumulates in the brains of individuals with Alzheimer disease (AD). 2 key findings →
Evidence: low
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Sex or gender differences in the risk of Alzheimer's disease and related dementias (ADRD) differ by world region, suggesting that there are potentially modifiable risk factors for intervention. 1 key finding →
Evidence: low
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Several potential disease-modifying drugs for Alzheimer's disease (AD) have failed to show any effect on disease progression in clinical trials, conceivably because the AD subjects are already too advanced to derive clinical benefit from treatment and because diagnosis based on clinical criteria alone introduces a high misdiagnosis rate. 1 key finding →
Evidence: low
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Young adults typically deactivate specific brain regions during active task performance. 2 key findings →
Participants: 32 Evidence: low
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Cross-sectional and longitudinal observation. 2 key findings →
Design: cross-sectional Evidence: moderate
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Demographic and clinical factors impact PD survival. 4 key findings →
Design: cohort study Evidence: moderate
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While a growing body of evidence points to potentially modifiable individual risk factors for dementia, the built and social environments in which people develop and navigate cognitive decline are largely overlooked. 2 key findings →
Participants: 21,151 Evidence: low
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The findings suggest that GPS driving may serve as an effective and accurate digital biomarker for identifying preclinical AD among older adults. 2 key findings →
Participants: 64 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. 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events