We included 400 middle-aged CU participants, of whom 135 (33.8%) were CSF Aβ-positive. 5 key findings →
Design: cross-sectional Participants: 400 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
In participants who progressed to amyloid-positive MCI, plasma p-tau181/Aβ42 and GFAP diverged from stable controls earliest (about 13 and 12 years before symptom onset, respectively), followed by Aβ42/Aβ40, p-tau181, and NfL, all of which became abnormal before symptom onset. 4 key findings →
Design: longitudinal study Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
68/100
Across cohorts, the main biomarker associated with α-synuclein positivity at baseline was higher levels of Aβ pathology (all p values ≤ 0.02), but not tau. 5 key findings →
Design: cross-sectional Participants: 2,315 Evidence: moderate
Full summary, score breakdown and related studies → Original source
SAA+ individuals had faster cognitive decline than SAA-, notably in mild cognitive impairment, and presented with earlier symptom onset. 5 key findings →
Design: cross-sectional Participants: 1,637 Evidence: moderate
Full summary, score breakdown and related studies → Original source
67/100
Several promising plasma biomarkers for Alzheimer's disease have been recently developed, but their neuropathological correlates have not yet been fully determined. 2 key findings →
Design: longitudinal study Participants: 105 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This large study shows the role of plasma biomarkers in differentiating patients with different dementias, and at monitoring longitudinal change. 5 key findings →
Design: longitudinal study Participants: 300 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Data from 362 study participants were analyzed (mean [SD] age, 65.6 [7.9] years), of whom 152 (42.0%) were African American, 230 (63.5%) were women, and 189 (52.2%) had MCI. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results demonstrate the feasibility and potential of immunoassay-based multiplexing to provide a comprehensive view of AD-associated proteomic changes, consistent with the recently revised biological and diagnostic framework. 5 key findings →
Design: cross-sectional Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma Aβ42/Aβ40${{\rm A}\beta }_{42}/{{\rm A}\beta }_{40}$ may begin declining decades prior to brain amyloid accumulation, whereas p-tau ratios, GFAP, and NfL increase closer in time. 1 key finding →
Design: longitudinal study Participants: 199 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) tau (total tau, T-tau), neurofilament light (NFL), and neurogranin (Ng) are potential biomarkers for neurodegeneration in Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study Participants: 93 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study confirms the role of NFL as a biomarker in ALS. 3 key findings →
Design: longitudinal study Participants: 94 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The development of blood-based biomarkers of Alzheimer's disease (AD) pathology as tools for screening the general population is essential, but persists controversies. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Astrocytes are the most abundant cell type in the human central nervous system, and they play an important role in the regulation of neuronal physiology. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Plasma markers can track biological change over time, with plasma pTau181 and GFAP markers showing longitudinal change in individuals with preclinical AD. 3 key findings →
Design: longitudinal study Participants: 373 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The use of PRSs may be beneficial for increased precision in risk estimates among APOE4 carriers. 3 key findings →
Design: cohort study Participants: 712 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A biomarker panel was identified that included markers significantly increased (cortisol, pancreatic polypeptide, insulinlike growth factor binding protein 2, β(2) microglobulin, vascular cell adhesion molecule 1, carcinoembryonic antigen, matrix metalloprotein 2, CD40, macrophage inflammatory protein 1α, superoxide dismutase, and homocysteine) and decreased (apolipoprotein E, epidermal growth factor receptor, hemoglobin, calcium, zinc, interleukin 17, and albumin) in AD. 5 key findings →
Design: longitudinal study Participants: 207 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated-tau181 (p-tau181) showed the potential for Alzheimer's diagnosis and prognosis, but its role in detecting cerebral pathologies is unclear. 3 key findings →
Design: cross-sectional Participants: 1,189 Evidence: low
Full summary, score breakdown and related studies → Original source
We developed and validated a novel ECL based sandwich immunoassay for the NfL protein in serum (NfL(Umea47:3)); levels in ALS were more than 20-fold higher than in controls. 2 key findings →
Design: longitudinal study Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Serum NFL is increased in ALS in comparison to other conditions and can serve as diagnostic and prognostic biomarker. 2 key findings →
Design: longitudinal study Participants: 124 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The core Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers; amyloid-β (Aß), total tau (t-tau), and phosphorylated tau (p-tau181), are strong indicators of the presence of AD pathology, but do not correlate well with disease progression, and can be difficult to implement in longitudinal studies where repeat biofluid sampling is required. 3 key findings →
Design: longitudinal study Participants: 54 Evidence: moderate
Full summary, score breakdown and related studies → Original source
High levels of Aβ42 and tau in both young controls and DS suggest these proteins are produced by normal physiological processes, whereas the changes seen in later life are consistent with emergence of pathological alterations. 4 key findings →
Design: longitudinal study Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Age was the strongest risk factor for progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
66/100
Plasma p-tau biomarkers had a greater diagnostic performance and larger effect sizes compared to t-tau and Aβ42/40 assays in detecting Aβ pathology. 5 key findings →
Design: cross-sectional Participants: 197 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We analysed 461 participants from the DABNI and SPIN cohorts. 5 key findings →
Design: cross-sectional Participants: 461 Evidence: low
Full summary, score breakdown and related studies → Original source
We found that plasma p-tau217 was more associated with cognitive performance than p-tau181 and p-tau231 and that this relationship was particularly strong for memory scores (TRIAD: βp-tau217 = -0.53, βp-tau181 = -0.35 and βp-tau231 = -0.24; BioFINDER-2: βp-tau217 = -0.52, βp-tau181 = -0.24 and βp-tau231 = -0.29). 4 key findings →
Design: cross-sectional Participants: 103 Evidence: moderate
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 695 studies in this tag that have a study page, 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.
- Early Alzheimer's Disease Screening Approach Using Plasma Biomarkers
- Serum neurofilament light chain level as a predictor of cognitive stage transition
- Longitudinal stability of CSF tau levels in Alzheimer patients
- Comparative analysis of plasma pTau217, NfL and eight modifiable risk scores for 11-year dementia prediction in the HUNT Study
- Data-driven decomposition and staging of flortaucipir uptake in Alzheimer's disease
- Plasma amyloid beta measurements - a desired but elusive Alzheimer's disease biomarker
- A positive Alzheimer's blood biomarker is not a diagnosis: the presence-primacy-permission framework for plasma p-tau217
- Alzheimer’s Disease Biomarkers and Future Decline in Cognitive Normal Older Adults
- Astrocyte Biomarkers in Alzheimer's Disease
- Diagnostic value of serum versus plasma phospho-tau for Alzheimer's 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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