None of the three plasma biomarker was associated with NPS at baseline. 5 key findings →
Design: longitudinal study Participants: 76 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Higher CSF NfL was associated with decreasing microstructural integrity and WMH. 5 key findings →
Design: longitudinal study Participants: 536 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This Swedish study of over 1,200 people with memory symptoms found that a blood test combining p-tau217 with an amyloid ratio (the 'Amyloid Probability Score 2') was far more accurate at identifying Alzheimer's disease than doctors' clinical judgment alone. 3 key findings →
Design: cross-sectional Participants: 1,213 Evidence: high
Full summary, score breakdown and related studies → Original source
The AD PRS model that was most predictive of AD diagnosis (even without APOE) was the liver AD PRS: n = 1,115; odds ratio = 2.15 (1.67-2.78), p = 3.62×10-9. 3 key findings →
Design: cohort study Participants: 1,115 Evidence: moderate
Full summary, score breakdown and related studies → Original source
67/100
CSF A beta(1-42) was the most sensitive biomarker for AD in the autopsy cohort of CSF samples: receiver operating characteristic area under the curve of 0.913 and sensitivity for AD detection of 96.4%. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Blood biomarkers indicative of Alzheimer's disease (AD) pathology are altered in both preclinical and symptomatic stages of the disease.
Full summary, score breakdown and related studies → Original source Free full text
Plasma GFAP discriminated AD dementia from normal cognition (adjusted mean difference = 0.90 standard deviation [SD]) and mild cognitive impairment (adjusted mean difference = 0.72 SD), and demonstrated superior discrimination compared to alternative plasma biomarkers. 4 key findings →
Design: cross-sectional Participants: 567 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Delirium is associated with cognitive decline and subsequent dementia, and rises in plasma total tau (tTau) and neurofilament light (NfL), providing links to Amyloid-Tau-Neurodegeneration (ATN) pathophysiology. 4 key findings →
Design: cohort study Participants: 54 Evidence: moderate
Full summary, score breakdown and related studies → Original source
63/100
NfL demonstrated fair to excellent accuracy in differentiating non-ACS from CU groups (area under the curve [AUC], 0.79 to 0.94). p-tau217 had the highest accuracy for identifying Aβ (AUC 0.94) and tau positron emission tomography status (AUC 0.91). 5 key findings →
Participants: 2,984 Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to non-carriers, APOE ε4 carriers had lower Aβ42/Aβ40 and greater longitudinal increases in p-tau181 and GFAP; in contrast, the AD-PRS (excluding the APOE region) was associated with greater declines in Aβ42/Aβ40 among APOE ε4 non-carriers. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Levels of CSF Aβ42 decreased in patients with BD who had an episode during follow-up (BD-E) (N = 22) compared to patients without an episode (BD-NE) (N = 25) during follow-up (P = 0.002). 5 key findings →
Design: case-control study Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source
61/100
Aβ-independent factors included hemoglobin and estimated glomerular filtration rate (eGFR) for p-tau217 and hemoglobin, eGFR, and triiodothyronine (T3) for GFAP and NfL. 5 key findings →
Participants: 2,935 Evidence: moderate
Full summary, score breakdown and related studies → Original source
58/100
A total of 1,345 individuals were included. 5 key findings →
Design: cohort study Participants: 1,345 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study reviewed the structure, function, analytical aspects, and age-dependent normal ranges of neurofilaments, providing a comprehensive overview of neurofilament light chain as a marker of axonal injury across various neurological disorders. 2 key findings →
Full summary, score breakdown and related studies → Original source Free full text
In CU individuals from the development cohort, the combination of p-tau217 and Aβ42/40 significantly improved diagnostic accuracy (AUC: ALZpath 0.937 vs. 0.905, MSD 0.901 vs. 0.861; p < 0.05, DeLong test; 95% CIs) and model fit (AIC /BIC, p < 0.001) compared to p-tau217 alone. 5 key findings →
Participants: 1,545 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Increased p-tau181 was observed for both ɛ4 carriers and non-carriers close to AD onset, but exclusively for ɛ4 carriers in the early preclinical groups (7- and 13-years pre-AD). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 322 participants with p-tau217, GFAP, and NfL analyses were stratified into the EOAD or FTD group based on their diagnosis. 5 key findings →
Design: cohort study Participants: 245 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
54/100
NfL had a stronger association than t-tau with clinical scales; t-tau did not hold additional information to that given by NfL (P > 0.05 at all time points). 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
In single predictor models, p-tau231 (AUC = 0.87, p = 0.005) and GFAP (AUC = 0.87, p = 0.01) were associated with amyloid positivity, and p-tau231 remained significant in all multi-predictor models (p-values < 0.02). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Phosphorylated tau 181 (p-tau181), phosphorylated tau 231 (p-tau231), neurofilament light (NfL), and glial fibrillary acidic protein (GFAP) concentrations were unchanged both when stored at +4°C and +18°C. Amyloid-β 40 (Aβ40) and amyloid-β 42 (Aβ42) concentrations were stable for 24 h at +4°C but declined when stored at +18°C for longer than 6 h. This decline did not affect the Aβ42/Aβ40 ratio. 5 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
CRM-adjusted Aβ42 calibrator concentrations were calculated using the regression equation Y (CRM-adjusted) = 0.89X (calibrators) + 32.6. 5 key findings →
Participants: 766 Evidence: low
Full summary, score breakdown and related studies → Original source
P‐tau181 in CSF and plasma predicted tau accumulation (r > 0.36, P < .001), even in AD‐continuum individuals with normal baseline tau‐PET (A+T–; r > 0.37, P < .05). 4 key findings →
Participants: 163 Evidence: low
Full summary, score breakdown and related studies → Original source
Of the 250 participants, 121 (48.4%) were female and the mean age at follow-up was 76.06 (SD 0.48). 5 key findings →
Design: cohort study Participants: 250 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) neuropathology is extremely heterogeneous, and the evolution from preclinical to mild cognitive impairment until dementia is driven by interacting genetic/biological mechanisms not fully captured by current clinical/research criteria. 2 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Worse overall and local LC-EC integrity, indicated by lower fractional anisotropy (FA) and higher mean diffusivity (MD), was related to elevated concentrations of plasma phosphorylated tau 181 (p-tau181), p-tau217, and glial fibrillary acidic protein (GFAP). 5 key findings →
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
- 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →