Participants with higher total-tau and NfL at baseline had a higher risk of stroke and several stroke subtypes. 5 key findings →
Participants: 379 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Participants with higher total-tau and NfL at baseline had a higher risk of stroke and several stroke subtypes. 5 key findings →
Participants: 379 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our results support the utility of CSF VEC as a marker of endothelial injury in AD and highlight the importance of endothelial injury as an early pathology that contributes to cognitive impairment in even the earliest preclinical stages. 3 key findings →
Participants: 700 Evidence: moderate
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Twenty-seven individuals (14%) had an abnormal amyloid PET, and 14 twin-pairs (15%) showed discordant amyloid PET scans. 2 key findings →
Participants: 126 Evidence: low
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Comparing clinical stages, CSF PDGFRβ levels were increased at the MCI stage (Cohen's d = 0.55 [CI 95% 0.066, 1.0], P = 0.025) compared with NC. 3 key findings →
Participants: 23 Evidence: low
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Our findings suggest that microglial and astrocyte reactivity, measured through fluid biomarkers, occur early and impact the amyloid cascade on the preclinical Alzheimer´s continuum. 4 key findings →
Evidence: moderate
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We found that ML-PRS approaches improved upon standard PRS for prediction of AD endophenotypes, partly related to improved accounting for nonlinear effects of genetic susceptibility alleles. 3 key findings →
Participants: 1,791 Evidence: low
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Magnetic resonance spectroscopy detects Alzheimer's disease related inflammation and neurodegeneration, and could be a good noninvasive disease-stage biomarker in Down syndrome. 3 key findings →
Participants: 118 Evidence: moderate
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There is growing evidence that cognitive decline can be affected by both nutritional aspects and inflammation. 3 key findings →
Design: cross-sectional Participants: 116 Evidence: low
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Across 3 study samples, combining the functional connectome and molecular properties substantially enhanced the explanatory power compared to single modalities, providing a valuable tool to explain regional susceptibility to tau deposition in AD. 3 key findings →
Participants: 1,000 Evidence: low
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Determining blood biomarkers represents less invasive and less costly diagnostics for Alzheimer´s disease. 1 key finding →
Design: meta-analysis Evidence: high
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High correlations between plasma and serum were observed for most assays (ρ > 0.8), though plasma often yielded higher concentrations. 5 key findings →
Participants: 100 Evidence: low
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The final study sample comprised 8,797 participants (53.5% women, mean age at HUNT4 77.8 [SD 6.2]). 5 key findings →
Participants: 8,797 Evidence: low
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The study included 197 patients in whom lecanemab infusions had been started (lecanemab group), as well as 173 patients in whom lecanemab had been ordered but not yet started, who were combined with 1139 research participants with cognitive impairment from the Knight ADRC cohort to form the untreated control group with cognitive impairment (n=1312). 5 key findings →
Design: cohort study Participants: 1,312 Evidence: moderate
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Neurofilament light chain (NfL) is a potential diagnostic and prognostic plasma biomarker for numerous neurological diseases including Alzheimer's disease (AD). 1 key finding →
Participants: 350 Evidence: low
Full summary, score breakdown and related studies → Original source
NDs share a CSF profile characterized by increased levels of CSF CHIT1, YKL-40, and GFAP, which likely reflects a common neuroinflammatory response to protein misfolding and aggregation. 3 key findings →
Participants: 101 Evidence: low
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We found that pharmacological activation of PPARA by the PPARA agonists gemfibrozil and Wy14643 induces autophagy in human microglia (HM) cells and U251 human glioma cells stably expressing the human APP (amyloid beta precursor protein) mutant (APP-p.M671L) and this effect is PPARA-dependent. 2 key findings →
Evidence: low
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Astrocytes are a population of cells with distinctive morphological and functional characteristics that differ within specific areas of the brain. 1 key finding →
Evidence: low
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Plasma neurofilament light (NFL) has been proposed as a blood-based biomarker for neurodegeneration in Alzheimer's disease (AD) and parkinsonian disorders. 2 key findings →
Evidence: low
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Higher gLFC connectivity is a functional substrate of CR that helps to maintain episodic memory relatively well in the face of emerging FDG-PET hypometabolism in early-stage AD. 3 key findings →
Evidence: low
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Lewy body (LB) disorders, including Parkinson disease (PD), Parkinson disease dementia (PDD), and dementia with Lewy bodies (DLB), are the second most common type of neurodegenerative dementia. 2 key findings →
Design: longitudinal study Evidence: moderate
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Molecular subtypes of sporadic CJD show different levels of plasma tau. 2 key findings →
Participants: 132 Evidence: low
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Alzheimer's disease (AD), the most common form of dementia, remains challenging to understand and treat despite decades of research and clinical investigation. 3 key findings →
Evidence: low
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Concordance between scan results and baseline diagnosis was high (PiB 84%, FDG 82%). 4 key findings →
Participants: 24 Evidence: low
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The Study of Knowledge and Reactions to Amyloid Testing, a substudy of an AD prevention trial, involved 2 semistructured telephone interviews with 80 participants recruited from 9 study sites: 50 received elevated and 30 received not elevated amyloid PET scan results. 5 key findings →
Participants: 80 Evidence: low
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CSF NfL is a non-specific marker of aging and white matter integrity with limited sensitivity to specific markers of AD. 4 key findings →
Participants: 71 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →