The study included 57 patients (54% female, mean age 67 years), of whom 41 met AD diagnostic criteria. 5 key findings →
Participants: 57 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma tau was higher in patients with AD than cognitively normal controls (P < .001, area under the receiver operating characteristic curve = 0.79) similarly to CSF tau and CSF P-tau and was negatively correlated with cognition in AD. 5 key findings →
Participants: 68 Evidence: low
Full summary, score breakdown and related studies → Original source
After 20 years of follow-up, 123 patients (95%) were deceased. 5 key findings →
Participants: 129 Evidence: low
Full summary, score breakdown and related studies → Original source
Biofluid markers of phosphorylated tau181 (p-tau181) are increasingly popular for the detection of early Alzheimer's pathologic changes. 3 key findings →
Participants: 727 Evidence: low
Full summary, score breakdown and related studies → Original source
All measured CSF complement proteins were increased in AD versus CU subjects, with C4a displaying the most robust increase. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
There were significant differences in plasma p‐tau181 values between Controls and those with AD at all ages up to 85 years. 5 key findings →
Participants: 1,558 Evidence: low
Full summary, score breakdown and related studies → Original source
The National Institute on Aging-Alzheimer's Association (NIA-AA) guidelines for Alzheimer's disease (AD) propose the categorization of individuals according to their biomarker constellation. 1 key finding →
Participants: 41 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study identified the plasma biomarker analytes and assays that most accurately classified amyloid pathology and other AD-related outcomes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
P-tau isoforms can be measured robustly by several novel high-sensitive Simoa assays. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
HIGHLIGHTS: Different plasma phosphorylated tau (p-tau) species reflect different pathological processes of Alzheimer's disease (AD), with p-tau231 showing the greatest association with the earliest increases in brain amyloid beta (Aβ) accumulation, while p-tau217 shows greater association with both brain Aβ and early tau pathology, and other p-tau and tau fragment species show greater association with later stages of brain tau pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofilament light chain (NfL) is a novel biomarker of neurodegenerative diseases. 3 key findings →
Participants: 43 Evidence: low
Full summary, score breakdown and related studies → Original source
This mass spectrometry-based plasma biomarker test: has strong diagnostic performance; can accurately distinguish brain amyloid positive from amyloid negative individuals; may aid in the diagnostic evaluation process for Alzheimer's disease; and may enhance the efficiency of enrolling participants into Alzheimer's disease drug trials. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
It is possible to create a blood-based screening algorithm that works across both serum and plasma that provides a comparable screening accuracy to that obtained from CSF analyses. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is an urgent need for biomarkers in plasma to identify Alzheimer's disease (AD). 3 key findings →
Participants: 142 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings indicate that although plasma and CSF neurogranin may reflect the volume of acute cerebral ischemia, this synaptic protein is less likely to be a potential AIS biomarker. 4 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Diagnosis of the progressive neurodegenerative disorder Alzheimer's disease (AD) can only definitively be made postmortem. 4 key findings →
Participants: 270 Evidence: moderate
Full summary, score breakdown and related studies → Original source
An ideal diagnostic test for Alzheimer's disease (AD) should be non-invasive and easily applicable. 1 key finding →
Participants: 155 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. 3 key findings →
Participants: 88 Evidence: low
Full summary, score breakdown and related studies → Original source
All markers tracked neuropathological severity, with BD p-tau217 having larger fold-changes than p-tau217 but BD p-tau217/Aβ42 enhancing this further. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 was 57% higher in subjects with at least one APOE ε4 allele, increased with age, was higher in males, and negatively correlated with brain volume measures by magnetic resonance imaging. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The assay demonstrated strong analytical performance, with repeatability and intermediate precision (%CV < 7%) and an LLoQ of 0.12 pg/mL. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Movement disorders have been carefully clinically defined, based on clinico-pathological series; however there is often diagnostic and prognostic uncertainty, especially in early stage disease. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent dementia, but it shows similar initial symptoms to other neurocognitive diseases (Lewy body disease (LBD) and frontotemporal dementia (FTD)). 1 key finding →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Pairwise comparisons among the three groups showed that compared with the health checkup (HC) group, serum NfL and GFAP were increased in both AD and MCI (PNfL < 0.05, PGFAP < 0.01). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among diagnostic groups, highest plasma Nfl and t-tau concentrations were detected in CJD (fold changes of 38 and 18, respectively, compared to HC). 5 key findings →
Participants: 70 Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 707 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.
- False positive plasma p-tau217 results associated with heterophilic antibody interference: A potential clinical pitfall
- Associations of Alzheimer's-related plasma biomarkers with cognitive decline in Parkinson's disease
- Measurement batch differences and between-batch conversion of Alzheimer's disease cerebrospinal fluid biomarker values
- Association of plasma p-tau and p-tau/Aβ ratio with Alzheimer's pathology
- Plasma eMTBR-tau as a robust biomarker for Alzheimer’s disease tangle pathology up to 10 years before death
- CSF biomarkers for dementia
- Relationship of serum beta-synuclein with blood biomarkers and brain atrophy
- Evidence that iron accelerates Alzheimer's pathology: a CSF biomarker study
- CSF Alzheimer’s Disease Biomarkers in Relation to Functional Status and Tofersen Treatment Response in ALS
- Longitudinal cognitive and biomarker changes in dominantly inherited Alzheimer disease
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 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.
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 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 →