In addition to predicting MCI/AD, our model has been interrogated for potential genetic biomarkers using SHAP. 1 key finding →
Participants: 626 Evidence: low
Full summary, score breakdown and related studies → Original source
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
In addition to predicting MCI/AD, our model has been interrogated for potential genetic biomarkers using SHAP. 1 key finding →
Participants: 626 Evidence: low
Full summary, score breakdown and related studies → Original source
CCT causes functional and structural changes in extensive brain regions and improves cognitive function in older adults with MCI. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Hundreds of commonly expressed urinary EV proteins with stable expression over time were distinguished from proteins with high variability. 1 key finding →
Participants: 50 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We established AD diagnostic models using plasma biomarkers for Chinese participants. 2 key findings →
Participants: 159 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Determining blood biomarkers represents less invasive and less costly diagnostics for Alzheimer´s disease. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Clusters of CSF biomarker levels are related to cognitive profiles in Alzheimer disease. 1 key finding →
Participants: 177 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
None of the participants were diabetics, smokers, or met criteria for obesity. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The sensitivity of CSF-beta-amyloid(1-42) level as a diagnostic marker for AD is high. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Both Aβ and tau pathology affect default mode network integrity before clinical onset of Alzheimer disease. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cholinergic markers, neuropeptides, and amines and their metabolites were sampled from identical specimens across 10 neocortical regions in a large sample of Alzheimer's disease (AD) cases and controls. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Using a targeted proteomic screen, we identified novel candidate biomarkers that complement the best current CSF biomarkers for distinguishing very mildly/mildly demented from cognitively normal individuals. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We studied CSF-tau and CSF-Abeta42 in 16 patients with mild cognitive impairment (MCI) who at follow-up investigations 6-27 months later had progressed to Alzheimer's disease (AD) with dementia. 1 key finding →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This article presents recommendations, based on the Grading of Recommendations, Assessment, Development, and Evaluation method, for the clinical application of cerebrospinal fluid (CSF) amyloid-β 1-42 , tau, and phosphorylated tau in the diagnostic evaluation of patients with mild cognitive impairment (MCI). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's Disease Neuroimaging Initiative database. 4 key findings →
Participants: 57 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid angiopathy is caused by deposition of the amyloid beta protein in the cerebral vasculature. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patients with autopsy-confirmed LBD (n = 24) and autopsy-confirmed Alzheimer disease (AD) (n = 23) and cognitively normal (n = 36) controls were studied. 4 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To better understand how sleep/wake dysregulation affects Alzheimer's disease (AD), we compared the cerebrospinal fluid (CSF) orexin and histamine/tele-methylhistamine (HA/t-MHA) levels of 82 patients (41 probable-AD-high level of evidence, 41 mild cognitive impairment MCI-due-to-AD), 24 other neurologic disorders (OND) and 24 controls. 4 key findings →
Participants: 82 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Although typical forms of Alzheimer disease (AD) and Creutzfeldt-Jakob disease (CJD) are clinically distinguishable, atypical AD phenotypes may pose a diagnostic challenge. 4 key findings →
Participants: 82 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This prospective observational study included 22 patients with PCA who underwent CSF biomarker analysis of total tau (t-tau), phosphorylated tau on amino acid 181 (p-tau181), and amyloid β (Aβ(42)). 4 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The ability of Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers (amyloid β peptide 1-42, total tau, and phosphorylated tau) to discriminate AD from related disorders is limited. 4 key findings →
Participants: 367 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Irisin, released by muscles during exercise, was recently identified as a neuroprotective factor in mouse models of Alzheimer disease (AD). 4 key findings →
Participants: 82 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 939 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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