Two independent cohorts were used in this study. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Two independent cohorts were used in this study. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Frailty increasingly is recognized as a factor that modifies the relationship between disease biomarkers, including neuropathology, and dementia expression. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Older age, White race, APOE ε4 carrier, and diabetes were associated with biomarker levels indicative of higher AD risk (lower Aβ42/40; higher p-tau217, p-tau217/Aβ42, NfL, and GFAP). 5 key findings →
Participants: 1,356 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among 871 participants (mean age: 62.80 ± 6.02 years), every SD increase in AIx and RI scores was both associated with 0.010 pg/mL (95% CI: 0.003–0.017, p = 0.004) higher blood p-tau217 levels after adjustment for age, employment status, BMI, mild cognitive impairment, hypertension, cholesterol-HDL ratio, renal function, and ApoE4 carrier status. 5 key findings →
Design: cross-sectional Participants: 871 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Contrast-induced nephropathy (CIN) represents a significant complication associated with the use of iodinated contrast media (ICM), especially in individuals with preexisting renal impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a growing global health concern that significantly impacts the quality of life for millions of individuals and imposes substantial burdens on healthcare systems. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There has been growing interest in the role of biofluid biomarkers to aid the diagnosis of dementia in older people. 1 key finding →
Participants: 46 Evidence: low
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AcTau174 levels were elevated in all dementia groups compared to controls, with a stepwise increase from controls to MCI-AD (2.2-fold) to AD dementia (3.5-fold, Figure 1). 5 key findings →
Evidence: moderate
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Physical activity was not associated with plasma Aβ42/Aβ40, p-tau217, or brain Aβ burden 7 years later. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Major systemic diseases elevate AMD risk, compounded by comorbidities. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal lobar degeneration (FTLD) is the second most common early-onset dementia. 3 key findings →
Participants: 25 Evidence: low
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The development of cerebrospinal fluid and blood-based biomarkers for Alzheimer disease (AD) and related disorders is rapidly progressing. 5 key findings →
Evidence: low
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Glial fibrillary acidic protein (GFAP) is the structural protein of the astroglial intermediate filament that forms the morphological basis of astrogliosis. 2 key findings →
Participants: 39 Evidence: low
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We conclude that an inverse correlation between levels of inflammation in cortical areas and plasma NfL levels indicates that microglial activation may initially be protective to axons in AD. 3 key findings →
Evidence: low
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The human GFAP splice variants GFAPDelta164 and GFAPDeltaexon6 both result in a GFAP protein isoform with a unique out-of-frame carboxy-terminus that can be detected by the GFAP+1 antibody. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common neurodegenerative disorder that leads to progressive cognitive decline and imposes a significant socio-economic burden. 1 key finding →
Evidence: low
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Prior work on the link between blood-based biomarkers and cognitive status has largely been based on dichotomous classifications rather than detailed neuropsychological functioning. 1 key finding →
Participants: 395 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In conclusion the analysis of oxysterols in plasma and CSF seems to contribute to investigate the role of cholesterol metabolism in pathogenesis of neurodegeneration and is helpful in the study of patients affected by neurodegenerative diseases. 1 key finding →
Evidence: low
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The increasing prevalence of Alzheimer's disease and the devastating consequences of late-life dementia motivates the drive to develop diagnostic biomarkers to reliably identify the pathology associated with this disorder. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Numerous studies have shown a marked decrease of beta-amyloid(42) (Abeta(42)) in the cerebrospinal fluid (CSF) of patients with incipient Alzheimer's disease (AD). 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Increasing evidence suggests that free radical-mediated oxidation of biological substrates is a key feature of Alzheimer's disease (AD) pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The amyloid beta protein (A beta), a 4 kD fragment of the beta amyloid precursor protein, is deposited as insoluble amyloid in the brain of Alzheimer disease (AD) subjects. 4 key findings →
Evidence: low
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This article gives an updated account of the clinical application of cerebrospinal fluid (CSF) biomarkers for Alzheimer disease (AD). 2 key findings →
Evidence: low
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Standard markers in cerebrospinal fluid (CSF), as soluble amyloid beta 1-42 (Abeta1-42) and total tau protein (t-tau), may contribute to dementia subtypes diagnostic accuracy. 4 key findings →
Evidence: low
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The AD subjects showed positive correlations between CSF-T-tau and CSF-P-tau versus CSF-Mn (r(s) = 0.22, p = 0.004; r(s) = 0.18, p = 0.021). 4 key findings →
Participants: 264 Evidence: low
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10 of the 3,069 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →