31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We tested the hypothesis that plasma neurofilament light chain (NfL) identifies asymptomatic carriers of familial frontotemporal lobar degeneration (FTLD)-causing mutations at risk of disease progression. 4 key findings →
Design: longitudinal study Participants: 277 Evidence: moderate
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When identifying participants with abnormal CSF Aβ42/40 in the whole cohort, plasma IP-MS-WashU Aβ42/40 showed significantly higher accuracy (area under the receiver operating characteristic curve [AUC], 0.86; 95% CI, 0.81-0.90) than LC-MS-Arc Aβ42/40, IA-Elc Aβ42/40, IA-EI Aβ42/40, and IA-N4PE Aβ42/40 (AUC range, 0.69-0.78; P Conclusions and relevance The results from 2 independent cohorts indicate that certain MS-based methods performed better than most of the immunoassays for plasma Aβ42/40 when detecting brain Aβ pathology. 2 key findings →
Participants: 182 Evidence: moderate
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Advances in molecular positron emission tomography (PET) have enabled anatomic tracking of brain pathology in longitudinal studies of normal aging and dementia, including assessment of the central model of Alzheimer's disease (AD) pathogenesis, according to which TAU pathology begins focally but expands catastrophically under the influence of amyloid-β (Aβ) pathology to mediate neurodegeneration and cognitive decline. 2 key findings →
Design: longitudinal study Participants: 104 Evidence: moderate
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Plasma Aβ42/Aβ40 is a robust measure for detecting amyloid plaques and can be utilized to aid in the diagnosis of AD, identify those at risk for future dementia due to AD, and improve the diversity of populations enrolled in AD research and clinical trials. 3 key findings →
Participants: 465 Evidence: moderate
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We found that longitudinal changes in cognitive function measured by the cognitive composite decreased at low and high values of total sleep time (P < 0.001), time in non-REM (P < 0.001) and REM sleep (P < 0.001), sleep efficiency (P < 0.01) and <1 Hz and 1-4.5 Hz non-REM slow wave activity (P < 0.001) even after adjusting for age, CSF total tau/amyloid-β42 ratio, APOE ε4 carrier status, years of education and sex. 2 key findings →
Design: cross-sectional Participants: 100 Evidence: moderate
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The genetic basis of Lewy body dementia (LBD) is not well understood. 4 key findings →
Evidence: low
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The data set included 18 178 patients, of which 10 991 (60.5%) had MCI and 7187 (39.5%) had dementia (mean [SD] age, 75.8 [6.3] years; 9333 women [51.3%]). 3 key findings →
Design: cross-sectional Participants: 18 Evidence: low
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Due to trisomy of chromosome 21 and the resultant extra copy of the amyloid precursor protein gene, nearly all adults with Down syndrome develop Alzheimer's disease pathology by the age of 40 years and are at high risk for dementia given their increased life expectancy compared with adults with Down syndrome in the past. 1 key finding →
Design: cross-sectional Participants: 41 Evidence: moderate
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Compared with men, women had decreased risk of any LEA (hazard ratio [HR], 0.34 [95% CI, 0.31-0.37]). 5 key findings →
Design: cohort study Evidence: moderate
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Alzheimer's disease is characterized by β-amyloid plaques and tau tangles. 4 key findings →
Participants: 88 Evidence: moderate
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Alzheimer's disease (AD) is the most prevalent cause of dementia 1 . 4 key findings →
Evidence: low
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This Primer conceptualizes Alzheimer disease (AD) as a genetic and sporadic neurodegenerative disorder driven by a complex interplay between loss of synaptic homeostasis and endosomal/lysosomal clearance pathway dysfunction, in which Aβ and tau products play key roles. 4 key findings →
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CSF Aβ 42 and PiB PET showed maximal correlation when collected within 6 years of each other ( R ≈ -0.5). 1 key finding →
Design: longitudinal study Participants: 371 Evidence: moderate
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A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA). 3 key findings →
Design: longitudinal study Evidence: moderate
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The reference standard for amyloid-PET quantification requires structural MRI (sMRI) for preprocessing in both multi-site research studies and clinical trials. 4 key findings →
Participants: 740 Evidence: low
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Macrophage-mediated inflammation is critical in the pathogenesis of non-alcoholic steatohepatitis (NASH). 4 key findings →
Evidence: low
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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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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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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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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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In Alzheimer's disease (AD) models, AD risk variants in the microglial-expressed TREM2 gene decrease Aβ plaque-associated microgliosis and increase neuritic dystrophy as well as plaque-associated seeding and spreading of tau aggregates. 4 key findings →
Evidence: low
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The Electrophysiology Professional Interest Area (EPIA) and Global Brain Consortium endorsed recommendations on candidate electroencephalography (EEG) measures for Alzheimer's disease (AD) clinical trials. 3 key findings →
Evidence: low
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Neither fibrillar nor nonfibrillar Aβ content alone sufficed to explain the Aβ PET findings in either AD model. 5 key findings →
Design: longitudinal study Evidence: moderate
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The hemizygous R47H variant of triggering receptor expressed on myeloid cells 2 ( TREM2 ), a microglia-specific gene in the brain, increases risk for late-onset Alzheimer’s disease (AD). 4 key findings →
Evidence: low
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Mycobacterial cell-wall glycolipids elicit an anti-mycobacterial immune response via FcRγ-associated C-type lectin receptors, including Mincle, and caspase-recruitment domain family member 9 (CARD9). 4 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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