27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurodegenerative diseases are a growing burden, and there is an urgent need for better biomarkers for diagnosis, prognosis, and treatment efficacy. 5 key findings →
Participants: 197 Evidence: low
Full summary, score breakdown and related studies → Original source
Robust and accessible biomarkers that can capture the heterogeneity of Alzheimer's disease and its diverse pathological processes are urgently needed. 2 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
The participants comprising the AIBL cohort represent a group of highly motivated and well-characterized individuals who represent a unique resource for the study of AD. 1 key finding →
Participants: 1,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source
ALS plasma showed elevation of the established biomarkers, neurofilament light chain (NEFL) and neurofilament heavy chain (NEFH). 5 key findings →
Participants: 86 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 was accurate for discriminating between Core1+ and Core1- patients (area under the curve = 0.92) with an optimal cut-off value of 0.274 pg/mL, revealing good accuracy (86.29%), positive predictive value (PPV; 88.18%), and negative predictive value (NPV; 83.09%). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
p-Tau217 levels were highest in patients with Alzheimer's disease (AD) dementia, whereas NfL levels were highest in patients with frontotemporal dementia (FTD). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
On NULISA, phosphorylated tau (p-tau217, p-tau231, and p-tau181), glial fibrillary acidic protein (GFAP), and microtubule-associated protein tau (MAPT-tau) showed the top significant association with amyloid beta (Aβ) positron emission tomography (PET) status, followed by the neuroinflammation markers C-C motif ligand 2 (CCL2), chitotriosidase 1 (CHIT1) and interleukin-8 (CXCL8), and the synaptic marker neurogranin (NRGN). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a debilitating neurodegenerative disorder characterized by brain aggregation of β-amyloid (Aβ) peptides and phosphorylated tau (P-tau) proteins. 3 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
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
Lower cerebrospinal fluid (CSF) ApoE, higher CSF p-tau181/amyloid-β (Aβ)42, and higher plasma p-tau231/Aβ42 were associated with higher variability of sleep midpoint, sleep duration, and/or activity count. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
After the median time of incident TBI, Aβ42/Aβ40 levels remained lower for 9.3 years, and pTau181, NfL, and GFAP remained elevated for 8.5, >13.8, and 12.7 years, respectively. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CBS Aβ+ group showed a reduced Aβ42/40 ratio, with elevated phosphorylated tau (p-tau)181, glial fibrillary acidic protein (GFAP), and neurofilament light (NfL) concentrations, while CBS Aβ- group only showed elevated NfL concentration compared to CU. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
There has been a rapid growth in research on peripheral fluid biomarkers for Alzheimer's disease (AD) and AD-related dementias, because they are non-invasive, relatively inexpensive and easily accessible. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Asthma participants had widespread and large-magnitude differences in several dMRI metrics, which were indicative of neuroinflammation and neurodegeneration, and which were robustly associated with GFAP and, to a lesser extent, NfL. 5 key findings →
Participants: 111 Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormal levels of plasma glial fibrillary acidic protein (GFAP) were found at the prodromal stage of MCI-LB in association with increased amyloid PET. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The common marmoset (Callithrix jacchus), a small South American monkey, is an important nonhuman primate model in the study of aging and age-related neurodegenerative disease, including Alzheimer's disease, Parkinson's disease, and related dementias. 1 key finding →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers of neurodegeneration demonstrate great promise for the diagnosis and prognosis of Alzheimer's disease. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Discrimination of disease-related interactions of the core subsystem and FPN was found in AD-spectrum patients, which was the neural circuit fundamental to plasma NFL disrupting cognitive integrity. 3 key findings →
Participants: 112 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma neurofilament light chain (NfL)'s link to dementia may be mediated through white matter integrity (WMI). 2 key findings →
Participants: 163 Evidence: low
Full summary, score breakdown and related studies → Original source
NFL discriminated patients from controls with an area under the curve of 0.914 (95% CI, 0.843-0.984; p < 0.001) (cut-off: 76.46 pg/mL; 94% sensitivity, 76.9% specificity). 5 key findings →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Testing an Alzheimer's disease continuum cohort, the area under the curve (AUC), sensitivity, specificity, and accuracy for the p-tau217/Aβ42 ratio reached 0.961, 93%, 92%, and 93%, respectively. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among the hip fracture patients, 88.6% of the cognitively normal (Clinical Dementia Rating-CDR 0; n = 70) and 98.8% with mild cognitive impairment (CDR 0.5; n = 81) fell in the abnormal biomarker categories by the A/T/N classification. 3 key findings →
Participants: 70 Evidence: low
Full summary, score breakdown and related studies → Original source
Studying the correlation between cerebrospinal fluid (CSF) metabolites and the Alzheimer's Disease (AD) biomarkers may offer a window to the alterations of the brain metabolome and unveil potential biological mechanisms underlying AD. 4 key findings →
Participants: 338 Evidence: low
Full summary, score breakdown and related studies → Original source
Β-site amyloid precursor protein (APP) cleaving enzyme (BACE1) is a crucial protease in the production of amyloid-β (Aβ) in Alzheimer's disease (AD) patients. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma amyloid-β (Aβ) was associated with brain Aβ deposition and Alzheimer's disease (AD) development. 4 key findings →
Participants: 449 Evidence: low
Full summary, score breakdown and related studies → Original source
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.
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
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.
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.
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 →