CSF NPTX2 and serum GFAP levels varied most between diagnostic groups. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
SerpinA1 (α1-antitrypsin) is a soluble glycoprotein, the cerebrospinal fluid (CSF) isoforms of which showed disease-specific changes in neurodegenerative disorders that are still unexplored in Alz-heimer’s disease (AD). 3 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
This study aimed to investigate the interaction between weight loss (WL) and plasma amyloid-β 42/40 (Aβ 42/40), neurofilament light chain (NfL), progranulin, and their association with cognitive decline over time among older adults. 4 key findings →
Participants: 470 Evidence: low
Full summary, score breakdown and related studies → Original source
After adjustment, only plasma p‐tau181 and NfL were significantly elevated in Aβ+ Obj‐SCD participants compared to Aβ− NC group. 5 key findings →
Participants: 234 Evidence: low
Full summary, score breakdown and related studies → Original source
54/100
The determination of cut-off points of core AD CSF biomarkers for the participating centers allows a better diagnostic accuracy. 1 key finding →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source
Higher grey matter volumes/cortical thickness and fluorodeoxyglucose uptake have been consistently found in cognitively unimpaired individuals with abnormal Alzheimer's disease biomarkers compared with those with normal biomarkers. 4 key findings →
Participants: 319 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The combination of amyloid and tau PETs was associated with changes in management and diagnosis of MCI and dementia, and the second-generation tau PET has a strong impact on the changes in diagnosis and management in memory clinics. 5 key findings →
Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Higher sNfL concentrations were associated with worse performance in cognitive tests at baseline, including CERAD (B = −10.084, SE = 2.999, p < 0.001) and MMSE (B = −3.014, SE = 1.293, p = 0.021). 3 key findings →
Design: cross-sectional Participants: 237 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Aβ misfolding and GFAP showed a strong ability to predict clinical AD risk and may be important early AD risk markers. 1 key finding →
Participants: 68 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF Aβ42/40 ratio can predict PET amyloid positivity with high accuracy in patients with a range of cognitive disorders when evaluating Aβ pathology independent of tau and neurodegeneration for research purposes. 4 key findings →
Participants: 44 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma and CSF AD biomarkers may perform similarly across diverse populations but future studies in large, diverse cohorts are needed. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau181 differentiates AD pathology cases from NC with high accuracy. 4 key findings →
Participants: 91 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Interpretation of axonal damage biomarker Neurofilament Light chain (NfL) concentrations is difficult due to the lack of age-specific and disease-specific reference values. 2 key findings →
Participants: 1,698 Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest a relationship between bone health and cognitive health. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Imaging of amyloid deposition using PET has been available in research studies for 2 decades and has been approved for clinical use by the U.S. Food and Drug Administration, the European Medicines Agency, and other regulatory agencies around the world. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study reveals an important role of astrocytic apoE3 and apoE4 on the deposition and accumulation of Aβ plaques as well as on certain Aβ-associated downstream effects. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We evaluated the relationship between baseline CSF p-tau181 and the rate of tau PET change in the temporal meta-ROI and entorhinal cortex (ERC) and how it varied by amyloid level (CSF Aβ42 or amyloid PET) among 143 individuals from the Mayo Clinic Study of Aging and Mayo Alzheimer Disease Research Center. 3 key findings →
Design: longitudinal study Participants: 143 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Creatinine and BMI are related to certain plasma biomarkers levels, but they do not have clinically relevant confounding effects for the vast majority of individuals. 1 key finding →
Participants: 748 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers related to amyloid, tau, and neurodegeneration (ATN) show great promise for identifying these pathological features of Alzheimer's Disease (AD) as shown by recent clinical studies and selected autopsy studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
All CSF p-tau biomarkers were accurate predictors of cognitive impairment but CSF p-tau217 demonstrated the largest fold-changes in AD patients in comparison to non-AD dementias and cognitively unimpaired individuals. 3 key findings →
Participants: 171 Evidence: low
Full summary, score breakdown and related studies → Original source
Carriers had higher plasma p-tau217 levels than non-carriers. 5 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
Brain amyloidosis differentiated several measures, especially EDTA plasma pTa u 181 A β 42 ( d = 1.29). 4 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source
To examine whether the type of blood collection tubes affects the quantification of plasma biomarkers for Alzheimer's disease analyzed with a single-molecule array (Simoa), we recruited a healthy cohort (n = 34, 11 males, mean age = 28.7 ± 7.55) and collected plasma in the following tubes: dipotassium ethylenediaminetetraacetic acid (K2-EDTA), heparin lithium (Li-Hep), and heparin sodium (Na-Hep). 1 key finding →
Participants: 34 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Different pipelines gave highly inter-correlated standardized uptake value ratios (SUVRs) (rho = 0.93-0.99). 5 key findings →
Participants: 23 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with dementia and is a serious concern for the health of individuals and government health care systems worldwide. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
- Randomized / 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
- Multicenter 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 32,180 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.
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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.
1,045 records (3.2% of the library) are not peer-reviewed — 966 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
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