T-tau, NfL, GFAP, and YKL-40 discriminated between diagnostic groups (receiver operating curve: 0.647-0.873). 5 key findings →
Participants: 1,193 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
After adjusting for age, plasma NfL level was higher in subjects with DAT (65.98±84.96 pg/mL), compared to in subjects with SCD (16.90±2.54 pg/mL) or MCI (25.53±10.42 pg/mL, p=0.004). 5 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Of 349 participants with available plasma data, 234 met inclusion criteria (31 controls, 141 in the training sample, and 62 in the validation sample). 5 key findings →
Design: cross-sectional Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source
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
64/100
NfL, Aβ40, Aβ42, GFAP, and p-tau181 were detected in all AH samples by Simoa platform. 5 key findings →
Design: cohort study Participants: 55 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
Pathophysiological substrate(s) and progression of Parkinson's disease (PD) with mild cognitive impairment (PD-MCI) are still matter of debate. 2 key findings →
Design: longitudinal study Participants: 48 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Participants were classified as hyposecretors (n = 22, median Aβ40 5,870.500 pg/mL, interquartile range [IQR] 1,431), normosecretors (n = 47, median Aβ40 10,817 pg/mL, IQR 3,622), and hypersecretors (n = 7, 19,767 pg/mL, IQR 3,088). 5 key findings →
Design: retrospective cohort Participants: 22 Evidence: moderate
Full summary, score breakdown and related studies → Original source
64/100
Family history (FH) of late-onset Alzheimer's disease (AD) is associated with changes in several cerebrospinal fluid (CSF) biomarkers in cognitively normal individuals. 2 key findings →
Design: longitudinal study Participants: 99 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Panama Aging Research Initiative is a cohort study of 423 adults aged ≥65 years recruited from an outpatient geriatric department of Panama's largest public hospital, the Social Security Fund's Dr Arnulfo Arias Madrid Hospital Complex (Complejo Hospitalario Dr Arnulfo Arias Madrid de la Caja de Seguro Social). 5 key findings →
Design: cohort study Participants: 423 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In subjects with biomarker-confirmed Alzheimer's pathology, high CSF ferritin (>6.2 ng/mL) was associated with accelerated depreciation of CSF Aβ1-42 (reporting increased plaque formation; p=0.0001). 5 key findings →
Design: longitudinal study Participants: 296 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Biomarkers were extracted from a total of 42 participants with longitudinal time points representing 164 imaging volumes. 5 key findings →
Design: longitudinal study Participants: 24 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Identifying which neuropsychological measures detect early cognitive changes associated with Alzheimer disease (AD), brain pathology would be helpful clinically for the diagnosis of early AD and for the design of clinical trials. 3 key findings →
Design: longitudinal study Participants: 233 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Intra- and inter-laboratory variability of cerebrospinal fluid (CSF) biomarker analyses remains an important issue. 1 key finding →
Design: longitudinal study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Carriers had lower LAS-FNAME performance (P < 0.001) and higher p-tau217 (P < 0.001), NfL (P = 0.013), and GFAP (P < 0.001) levels than non-carriers. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF was αSyn-SAA positive (αSyn+) in 36/80 AD patients (45%) and in 2/28 controls (7.1%). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is pathologically characterized by the accumulation of amyloid-β (Aβ) plaques, neurofibrillary tangles and widespread neuronal loss in the brain. 5 key findings →
Design: longitudinal study Participants: 12 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Elevated levels of AD biomarker p-tau181/Aβ42, by itself or combined with a low Aβ42/Aβ40 level, predicts clinically diagnosed AD. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Over 20% of patients with Alzheimer's disease (AD) worldwide are Chinese, although the efficacy of existing blood-based measures of AD biomarkers is largely unknown in Asian cohorts. 3 key findings →
Design: cross-sectional Participants: 425 Evidence: moderate
Full summary, score breakdown and related studies → Original source
To evaluate the clinical importance of cerebrospinal fluid (CSF) phosphorylated tau 181 (p-tau181) in mild cognitive impairment (MCI), Alzheimer's disease (AD) and other dementias, more specifically: frontotemporal degeneration (FTD), dementia with Lewy bodies (DLB), vascular dementia (VaD) and Parkinson's disease (PD) with dementia (PDD). 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
64/100
Relative to controls, greater Alzheimer's disease pathology (lower amyloid-β 42 /amyloid-β 40 , higher phosphorylated-tau-181) and synaptic degeneration (neurogranin) biomarker concentrations were associated with more adverse white matter metrics (e.g. lower neurite density, higher mean diffusivity) in patients with asthma. 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 and p-tau181 effectively predict Aβ+ among culturally different Asian populations. 1 key finding →
Participants: 270 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 measured using the Lumipulse platform shows promise as an accurate biomarker of preclinical AD pathology. 4 key findings →
Design: prospective cohort Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recently, conceptual systems for the in vivo staging of Alzheimer's disease (AD) using fluid biomarkers have been suggested. 4 key findings →
Participants: 219 Evidence: moderate
Full summary, score breakdown and related studies → Original source
64/100
Among the 128 study participants, the 104 patients with early PD had a different CSF pattern compared with the 13 patients with progressive supranuclear palsy (baseline area under the receiver operating characteristic curve, 0.87; P < .0001) and the 30 control participants (baseline area under the receiver operating characteristic curve, 0.69; P = .0021). 2 key findings →
Design: cohort study Participants: 104 Evidence: moderate
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 3,069 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.
- Blood Astrocyte Biomarkers in Alzheimer Disease: A Systematic Review and Meta-Analysis
- Blood-based biomarkers of cerebral small vessel disease
- Markers of neuroinflammation associated with Alzheimer's disease pathology in older adults
- Circulating Biomarkers of Neurodegeneration and All-Cause and Dementia-Specific Mortality
- Cerebrospinal fluid synaptosomal-associated protein 25 is a key player in synaptic degeneration in mild cognitive impairment and Alzheimer's disease
- Five Decades of Infusion Testing in Idiopathic Normal Pressure Hydrocephalus: A Biomarker in Search of a Gold Standard
- The association between cerebrospinal ferritin and soluble triggering receptor expressed on myeloid cells 2 along Alzheimer's continuum
- Arterial Spin-Labeling MRI Identifies Abnormal Perfusion Metric at the Gray Matter/CSF Interface in Cerebral Small Vessel Disease
- Soluble LR11 competes with amyloid β in binding to cerebrospinal fluid-high-density lipoprotein
- Plasma microRNA biomarker detection for mild cognitive impairment using differential correlation analysis
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →