Plasma biomarkers showed promising diagnostic performances and potential clinical usefulness in diagnosing dementia. 2 key findings →
Participants: 51 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
44/100
and amyloid composite in the context of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Non-core NfL and GFAP biomarkers are associated with both cross-sectional and longitudinal cognitive performance. 5 key findings →
Design: cross-sectional Participants: 334 Evidence: moderate
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BackgroundSystemic inflammation has been implicated in cognitive aging and neurodegeneration; however, inflammatory biomarkers are expressed in coordinated patterns rather than as isolated markers. 4 key findings →
Design: cross-sectional Participants: 334 Evidence: moderate
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A one‐point ALI increase was associated with MCI conversion odds by 15%. 1 key finding →
Participants: 385 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood-based biomarkers (BBMs) for Alzheimer disease (AD) offer widely expanded access to biomarker-informed diagnoses in community settings that have previously lacked such resources. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative condition representing the most common cause of dementia and currently affects millions of people worldwide. 5 key findings →
Design: narrative review Evidence: low
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KL -VSHET may help protect against amyloid pathology, particularly in the presence of APOE ε4, and regardless of APOE status in aMCI-AD. 5 key findings →
Participants: 223 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Glial fibrillary acidic protein (GFAP), a protein that is associated with 9-nm filaments of astrocytes, was observed to be increased in the astrocytes surrounding senile plaques in patients with Alzheimer dementia and in aged subjects without dementia. 2 key findings →
Evidence: low
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The association between an AD-like signature using the established biomarkers Aβ42, T-tau, and P-tau with increased levels of NFL provides in vivo evidence of an association between AD and subcortical axonal degeneration in this uniquely large dataset of CSF samples tested for dementia biomarkers. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We previously demonstrated that PNA5, a novel glycosylated angiotensin 1-7 (Ang-(1-7)) Mas receptor (MasR) agonist peptide, is an effective therapy to rescue cognitive impairment in our preclinical model of VCID. 5 key findings →
Participants: 15 Evidence: low
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SNfL was perceived as useful in 53% (n = 58) of the cases. 3 key findings →
Evidence: moderate
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Neurofilament light chain (NFL) has been recently introduced as a biomarker of early dementia. 18-Fluorodeoxyglucose positron emission tomography (18F-FDG-PET) is a proxy for regional hypometabolism in Alzheimer disease (AD). 1 key finding →
Participants: 149 Evidence: moderate
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We demonstrated a moderate positive correlation between PDGFRβ and both total Tau and phosphorylated Tau 181 in cognitively normal individuals. 4 key findings →
Design: cross-sectional Evidence: moderate
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With the introduction of the new causal amyloid targeting therapies, the role of biomarker-assisted diagnosis of Alzheimer disease (AD) has received a further boost. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
43/100
The white matter FC decreased in late MCI and AD dementia patients compared to CN participants, and this decrease was correlated with cognitive measures. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is accumulating evidence suggesting that changes in brain perfusion are present long before the clinical symptoms of Alzheimer's disease (AD), perhaps even before amyloid-β accumulation or brain atrophy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We compared proteomic profiles of CSF from individuals with FAD who were mutation carriers (MCs) and related noncarriers (NCs). 4 key findings →
Evidence: low
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Impairment in instrumental activities of daily living (IADL) heralds the transition from mild cognitive impairment (MCI) to dementia and is a major source of burden for both the patient and caregiver. 4 key findings →
Evidence: low
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Twenty-three patients with mild cognitive impairment (MCI), 12 dementia of Alzheimer's type (DAT), and 14 normal controls were studied following the ADNI2 protocol. 4 key findings →
Evidence: moderate
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The present study was aimed to investigate the relationships between thyroid stimulating hormone (TSH), freeT3 (fT3) and freeT4 (fT4) and brain glucose consumption as detectable by means of 2-deoxy-2-(F-18) fluoro-D-glucose (F-18 FDG) Positron Emission Tomography/Computed Tomography (PET/CT) in a selected population with Alzheimer disease (AD). 4 key findings →
Participants: 87 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is growing evidence that promising biomarkers of inflammation in Alzheimer´s disease (AD) and other neurodegenerative diseases correlate strongest to levels of tau or neurofilament, indicating an inflammatory response to neuronal damage or death. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood cadmium, lead, neurofilament light (NfL) chain, total tau (TTau), and amyloid beta (Aβ) 40 and Aβ42 concentrations were measured in 1516 participants in the Beaver Dam Offspring Study. 4 key findings →
Participants: 1,516 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E ε4 (APOE ε4) bring the higher risk of Alzheimer' Disease (AD). 4 key findings →
Participants: 1,610 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma biomarkers such as phospho-tau species are increasingly used in clinical practice for the diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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From across this tag
10 of the 830 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.
- [The role of CSF markers in the early diagnosis of Alzheimer's disease]
- Relationship between serum insulin-like growth factor-1 levels and Alzheimer's disease and vascular dementia
- Biofluid biomarker changes following treatment with sabirnetug (ACU193) in INTERCEPT-AD, a phase 1 trial in early Alzheimer's disease
- Population-based reference equations and Z-scores for blood biomarkers of neurodegenerative diseases
- Assessing Cognitive Decline and Dementia Risk in Black and White Older Adults With Blood Biomarkers pTau217, GFAP, NfL, and Aβ Ratio
- Biomarkers for early detection of Alzheimer disease
- Associations between plasma complement C1q and cerebrospinal fluid biomarkers of Alzheimer's disease pathology in cognitively intact adults: The CABLE study
- Age and diagnostic performance of Alzheimer disease CSF biomarkers
- Cerebrospinal Fluid Markers of Synaptic Injury and Functional Connectivity in Alzheimer Disease: Protocol for a Cross-Sectional Study
- Impaired lung function is associated with elevated blood biomarkers of AD/ADRD: unraveling the interplay with risk of dementia
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →