CSF p/t-tau ratio and NfL levels are strongly driven by ALS status. 1 key finding →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
CSF p/t-tau ratio and NfL levels are strongly driven by ALS status. 1 key finding →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Our objective was to evaluate the CSF phospho-Tau181/total-Tau (p/t-Tau) ratio to distinguish between the two main forms of frontotemporal lobar degeneration (FTLD): FTLD with TDP-43 (FTLD-TDP) and FTLD with Tau inclusions (FTLD-Tau). 2 key findings →
Participants: 39 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid and positron emission tomography biomarkers accurately predict an underlying Alzheimer's disease (AD) pathology; however, they represent either invasive or expensive diagnostic tools. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
The forms of tau in CSF and plasma are distinct, but in each specimen type, the levels of certain fragments are increased in AD. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is an urgent need to establish blood biomarkers for Alzheimer's disease (AD). 4 key findings →
Participants: 66 Evidence: low
Full summary, score breakdown and related studies → Original source
Despite a variety of testing approaches, it is often difficult to make an accurate diagnosis of Alzheimer's disease (AD), especially at an early stage of the disease. 2 key findings →
Participants: 74 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
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
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
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
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
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
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
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
The definition of Alzheimer's disease (AD) now considers the presence of the markers of amyloid (A), tau deposition (T), and neurodegeneration (N) essential for diagnosis. 2 key findings →
Participants: 172 Evidence: low
Full summary, score breakdown and related studies → Original source
The degree of PVS significantly increased with age in both, BG and CS regions independently of cardiovascular risk factors. 4 key findings →
Participants: 322 Evidence: low
Full summary, score breakdown and related studies → Original source
Twenty-nine percent of the cohort had Montreal Cognitive Assessment (MoCA) scores indicative of cognitive impairment or dementia after adjusting for age, sex, and education based on National Alzheimer's Coordinating Center normative data. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher CSF cortisol was associated with poorer global cognitive performance and higher disease severity at baseline. 5 key findings →
Participants: 145 Evidence: low
Full summary, score breakdown and related studies → Original source
The brain-derived neurotropic growth factor (BDNF) gene has been linked to dementia, inflammation, and Apolipoprotein E (APOE) ɛ4 status. 1 key finding →
Participants: 114 Evidence: low
Full summary, score breakdown and related studies → Original source
We investigated the effect of baseline Aβ, sex, and APOE on longitudinal tau accumulation in cerebrospinal fluid (CSF) in clinically normal older adults. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
10 of the 707 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 28,180 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →