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
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
These in vivo data support the role of Aβ pathology in the etiology and highlight the potential utility of CSF Aβ42 as an early prognostic biomarker of dementia associated with PD. 3 key findings →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Nine hundred and four participants (342 AD and 562 NAD) were studied; 400 in Mtp-1 and 504 in Mtp-2. 5 key findings →
Participants: 904 Evidence: low
Full summary, score breakdown and related studies → Original source
The present study creates the first-ever multiethnic referent sample that spans community-based and clinic-based populations for implementation of an AD blood screen. 1 key finding →
Participants: 1,329 Evidence: low
Full summary, score breakdown and related studies → Original source
A panel of structure- and concentration-based plasma amyloid biomarkers may predict conversion to clinical MCI and dementia due to AD in cognitively unimpaired subjects. 3 key findings →
Participants: 203 Evidence: moderate
Full summary, score breakdown and related studies → Original source
GFAP, NfL and pTau 181 levels in plasma were lower in SCD and MCI than in AD patients. 4 key findings →
Participants: 152 Evidence: low
Full summary, score breakdown and related studies → Original source
Two components were identified. Proinflammatory Component 2 was elevated in AD/MCI and in Black/African American participants, and strongly associated with poorer cognition (independently of neurofilament light [NfL], phosphorylated tau 217 [p-tau217], and glial fibrillary acidic protein [GFAP]). 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Analysis of cerebrospinal fluid (CSF) is one of the key tools for the state-of-the-art differential diagnosis of dementias. 3 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source
Discrepancies in diagnostic biomarkers for Alzheimer's Disease (AD) may arise from racial disparities, risk factors, or lifestyle differences. 2 key findings →
Design: cross-sectional 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
Beta-amyloid (Aβ 1-42 ) triggers the phosphorylation of tau protein in Alzheimer's disease (AD), but the relationship between phosphorylated tau (p-tau) and Aβ 1-42 in the blood is not elucidated. 4 key findings →
Participants: 62 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers of amyloid, tau, and neurodegeneration (ATN) need to be characterized in cognitively unimpaired (CU) elderly individuals. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
A combination of plasma Aβ42/Aβ40 and p-tau217 discriminated Aβ status with relatively high accuracy, whereas p-tau217 showed strongest associations with Aβ pathology in MCI but not in CU. 1 key finding →
Participants: 591 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
Plasma and CSF p-tau 217 had equivalent diagnostic performance for biomarker-defined AD. 2 key findings →
Participants: 174 Evidence: low
Full summary, score breakdown and related studies → Original source
In patients with a discrepancy between CSF p-tau181 and CSF Aβ42, the assessment of Aβ 42/40 ratio led to a reliable biological conclusion in over 50% of cases that agreed with a clinician's diagnosis. 1 key finding →
Participants: 367 Evidence: low
Full summary, score breakdown and related studies → Original source
Studies on markers of inflammation in subjects with mild cognitive impairment or AD dementia provided inconsistent results. 5 key findings →
Design: cross-sectional Participants: 48 Evidence: low
Full summary, score breakdown and related studies → Original source
We examined whether plasma p-tau181 and p-tau217 are specific biomarkers of pathologically confirmed Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
While cerebrospinal fluid (CSF) biomarkers are of use in the prediction and diagnosis of Alzheimer's disease our understanding of the background effects of age and the ApoE genotype is limited. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 and p-tau217/Aβ1-42 are effective diagnostic tools. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF-to-plasma transition will open new avenues for molecular phenotyping of Alzheimer's disease (AD). 5 key findings →
Participants: 173 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Low or decreasing plasma Aβ42 during the follow-up is associated with cognitive decline. 2 key findings →
Participants: 269 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is currently incurable, but there is general agreement that a minimally invasive blood biomarker for screening in preclinical stages would be crucial for future therapy. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Up to four freeze-thaw cycles do not influence single molecule array blood biomarkers of neurofilament light chain, total tau, or Aβ 42 , with at most minor reductions in Aβ 40 . 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 727 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.
- Comparative evaluation of clinical and cerebrospinal fluid biomarker characteristics in rapidly and non-rapidly progressive Alzheimer's disease
- Plasma phospho-tau181 in presymptomatic and symptomatic familial Alzheimer's disease: a longitudinal cohort study
- Plasma phosphorylated-tau181 as a predictive biomarker for Alzheimer's amyloid, tau and FDG PET status
- A positive Alzheimer's blood biomarker is not a diagnosis: the presence-primacy-permission framework for plasma p-tau217
- Plasma NfL and GFAP for predicting VCI and related brain changes in community and clinical cohorts
- Multicenter validation of plasma p-tau217/ amyloid beta 1-42 ratio in symptomatic Alzheimer's disease
- Integrating kidney function assessment into the clinical interpretation of plasma Alzheimer's disease biomarkers
- Combined use of plasma p-tau217, NfL, and GFAP predicts domain-specific cognitive decline in cognitively unimpaired and MCI individuals
- Multimer Detection System-Oligomerized Amyloid Beta (MDS-OAβ): A Plasma-Based Biomarker Differentiates Alzheimer's Disease from Other Etiologies of Dementia
- Plasma p-tau217 in Alzheimer's disease: Lumipulse and ALZpath SIMOA head-to-head comparison
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 →