Plasma pTau217 best identified amyloid-PET positivity (AUC > 0.91). 5 key findings →
Design: cross-sectional Evidence: moderate
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.
Most evidence on dementia risk factors comes from older or clinical samples, leaving their relation to normal cognitive aging unclear. 4 key findings →
Participants: 1,396 Evidence: moderate
Full summary, score breakdown and related studies → Original source
TSE showed stronger unadjusted associations than SUVR in selected region- and outcome-specific comparisons, supporting its potential as a complementary measure. 2 key findings →
Participants: 682 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers for Alzheimer disease and related dementias have been validated largely in populations of European ancestry. 4 key findings →
Participants: 786 Evidence: low
Full summary, score breakdown and related studies → Original source
Key Points Question Which candidate plasma proteins are associated with cognitive performance across multiple domains in older adults from the Democratic Republic of Congo? 5 key findings →
Design: prospective cohort Participants: 779 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma eMTBR-tau243 has been associated with tau pathology and cognitive decline. 3 key findings →
Design: cohort study Participants: 436 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The blood-based biomarker (BBM) profiles associated with genetic susceptibility to Alzheimer’s disease (AD) in general older populations remain poorly understood. 3 key findings →
Participants: 3,947 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid biomarkers sample distinct levels of an open, kinetically coupled biochemical system, yet scalar summaries may obscure biologically relevant configuration. 4 key findings →
Participants: 91 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 is elevated in αSynSAA-positive individuals at equivalent AD pathology measured by amyloid PET or the CSF ratio, and this elevation is attenuated most by fibrillar tau. 2 key findings →
Design: cross-sectional Participants: 193 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support plasma biomarkers for disease identification and risk stratification while underscoring the need for population□specific approaches. 4 key findings →
Participants: 3,645 Evidence: moderate
Full summary, score breakdown and related studies → Original source
ADNI identified task-dependent performance boundaries, particularly attenuated conditional T discrimination within A+. 2 key findings →
Design: post-hoc analysis Participants: 1,097 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Basal ganglia iron serves as a stage-dependent mediator linking pTau217 to hippocampal neurodegeneration, with prodromal AD potentially indicating a particularly vulnerable stage for iron-targeted interventions and iron profiling for patient stratification. 1 key finding →
Participants: 94 Evidence: low
Full summary, score breakdown and related studies → Original source
NOS1AP is an adaptor for neuronal nitric oxide synthase that engages several partner proteins and is implicated in Alzheimer’s disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Strong αSyn SAA positivity was detected in 24/443 patients with ALS (5.4%); overall positivity, including weak-positive samples, was 37/443 (8.4%). 5 key findings →
Design: longitudinal study Participants: 248 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We revealed graded, allele dosage‑dependent risk elevations for ACD, AD and VaD among APOE4 carriers, whereby homozygous carriers exhibited substantially higher incident dementia risk relative to heterozygous carriers and non‑carriers across all three clinical endpoints. 5 key findings →
Participants: 58,876 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based neurofilament light (NfL) is associated with all-cause mortality, but whether this reflects neuroaxonal injury or overlaps with cognitive and functional decline remains unclear. 3 key findings →
Participants: 559 Evidence: moderate
Full summary, score breakdown and related studies → Original source
16/100
In Phase 1 (n =176), inpatients with delirium showed higher concentrations of both NfL and GFAP than patients with dementia (β = 0.78; 95% CI [0.37, 1.20] and β = 0.39 [0.07, 0.73] respectively) or PPD groups (β = 1.17; [0.69, 1.66] and β = 0.83 [0.51, 1.24] respectively). 5 key findings →
Design: cross-sectional Participants: 176 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher pTau217 was associated with greater likelihood of developing dementia 11 years later. 5 key findings →
Participants: 3,935 Evidence: low
Full summary, score breakdown and related studies → Original source
Distinct biomarker associations with cognitive and emotional functioning support further longitudinal evaluation of BBMs for risk characterization in Latino older adults and potential disease monitoring applications. 3 key findings →
Design: longitudinal study Participants: 122 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Detection of the early phases of cognitive dysfunction is critical for identifying individuals at risk of neurodegeneration before irreversible damage occurs. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although endoplasmic reticulum (ER) stress and maladaptive unfolded protein response (UPR) are increasingly implicated in Alzheimer’s disease (AD), the influence of vitamin D (VitD) on these mechanisms remains unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Interventions targeting lifestyle and health behaviors support cognition in older adults at risk of dementia. 5 key findings →
Participants: 1,260 Evidence: high
Full summary, score breakdown and related studies → Original source
NOS1AP is a genetically validated driver of tau pathology in Alzheimer’s disease (AD), yet the NOS1AP-tau interaction itself has remained pharmacologically untargeted. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current biobanking guidelines require in-person blood collection and immediate processing for Alzheimer’s disease (AD) biomarker assessment. 4 key findings →
Participants: 43 Evidence: low
Full summary, score breakdown and related studies → Original source
Educational attainment and physical activity PRSs were associated with AD in both sexes. 5 key findings →
Design: systematic review Participants: 27,751 Evidence: high
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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