CCL23 is a chemokine implicated in inflammation and host defense responses. 4 key findings →
Design: cross-sectional Participants: 53 Evidence: moderate
Full summary, score breakdown and related studies → Original source
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
CCL23 is a chemokine implicated in inflammation and host defense responses. 4 key findings →
Design: cross-sectional Participants: 53 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Combinations of plasma and digital cognitive markers show promise for scalable diagnosis and prognosis of ADRD. 1 key finding →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
GFAP, NfL, and p-tau181 are valuable predictors of cognition and function across common neurodegenerative diseases, and may be useful in specialized clinics and clinical trials. 2 key findings →
Participants: 480 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The distribution of microbleeds revealed different associations with amyloid-β and phosphorylated tau 181 protein levels and cognition. 5 key findings →
Design: longitudinal study Participants: 626 Evidence: moderate
Full summary, score breakdown and related studies → Original source
An ECL immunoassay testing plasma P-tau217 accurately predicts amyloid PET positivity in cognitively unimpaired individuals. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma-to-autopsy studies are essential for validation of blood biomarkers and understanding their relation to Alzheimer's disease (AD) pathology. 2 key findings →
Participants: 123 Evidence: low
Full summary, score breakdown and related studies → Original source
LMW-specific p-tau assays could be more useful in the diagnostic workup of AD, especially in population-based communities where conditions causing peripheral neuropathy are frequent. 5 key findings →
Participants: 668 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers for screening may guide tau positrion emissition tomography (PET) scan referrals to optimize prognostic evaluation in Alzheimer's disease. 2 key findings →
Participants: 548 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma NfL levels objectively differentiates PD-MCI from PD-NC patients, and may serve as a plasma biomarker for predicting progression to dementia in PD. 3 key findings →
Design: prospective cohort Evidence: moderate
Full summary, score breakdown and related studies → Original source
These relatively non-invasive tests may be beneficial for clinical screening after replication in other populations and validation through neuroimaging or cerebrospinal fluid analysis. 2 key findings →
Participants: 787 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood biomarkers have emerged as accurate tools for detecting Alzheimer's disease (AD) pathology, offering a minimally invasive alternative to traditional diagnostic methods such as imaging and cerebrospinal fluid (CSF) analysis. 4 key findings →
Participants: 337 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 is an accurate indicator of amyloid pathology in a heterogeneous cohort and is superior to other plasma biomarkers assessed. 2 key findings →
Participants: 598 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study supported neuropsychiatric symptoms as early manifestations of preclinical Alzheimer's disease, and suggested plasma NfL to be a potential biomarker for detecting neuropsychiatric symptoms in Alzheimer's continuum. 3 key findings →
Design: cross-sectional Participants: 53 Evidence: low
Full summary, score breakdown and related studies → Original source
The innovative integrated models provide opportunity to assess Aβ pathology in a non-invasive and cost-effective way, which might facilitate AD-drug development, early screening, clinical diagnosis and prognosis evaluation. 2 key findings →
Participants: 609 Evidence: moderate
Full summary, score breakdown and related studies → Original source
PD patients who develop poor outcomes show lower DTI-ALPS, potentially reflecting impaired glymphatic clearance. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this sample, the high-throughput blood Aβ assay was not able to distinguish well between AD patients and controls. 2 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings indicate differential relationships between comorbidities (demographic, medical, diagnostic) across NHB, Hispanic, and NHW participants. 5 key findings →
Participants: 764 Evidence: moderate
Full summary, score breakdown and related studies → Original source
It is an open issue whether blood biomarkers serve to diagnose Alzheimer's disease (AD) or monitor its progression over time from prodromal stages. 2 key findings →
Design: longitudinal study Participants: 76 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings demonstrate that distinct inflammatory molecules are associated with different cognitive disorders. 5 key findings →
Participants: 131 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hippocampal subfields with distinctive atrophy patterns may mediate the effects of tau pathology on cognitive function. 2 key findings →
Design: cross-sectional Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source
Circulating metabolites can identify biochemical risk factors related to Alzheimer's disease (AD). 3 key findings →
Participants: 1,068 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease characterised by neuropathological hallmarks, including extracellular amyloid plaques and neurofibrillary tangles. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Highlights Mild behavioral impairment (MBI) is linked to elevated plasma p-tau217, a specific Alzheimer's disease biomarker.MBI increases the odds of plasma p-tau217 positivity in dementia-free individuals. 1 key finding →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status. 5 key findings →
Design: cohort Participants: 8,582 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Plasma GFAP and pTau biomarkers (pTau181, pTau231, pTau217) are significantly elevated in Aβ-positive individuals, with stronger Aβ–pTau associations observed in APOE ε4 carriers (CPAS: β = 0.26, p = 0.003 for pTau231; ADNI: β = 0.45, p < 0.001 for pTau181). 5 key findings →
Design: cohort Participants: 806 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 3,322 studies in this tag, 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 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 →