CSF p-tau217 was superior to p-tau181 for the diagnosis of Alzheimer's disease (AD) pathology. 4 key findings →
Participants: 753 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-tau217 was superior to p-tau181 for the diagnosis of Alzheimer's disease (AD) pathology. 4 key findings →
Participants: 753 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma was collected from 103 patients: 48 well-controlled (C, 31.3 % female) and 55 drug-resistant (DR, 50.9 % female). 5 key findings →
Participants: 103 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers were compared with densities of post-mortem-assessed amyloid plaques and neurofibrillary changes. 5 key findings →
Participants: 72 Evidence: moderate
Full summary, score breakdown and related studies → Original source
High CSF p-tau235 levels were strongly associated with CSF amyloidosis regardless of the clinical diagnosis, being significantly increased in MCI Aβ+ and dementia Aβ+ when compared with all other Aβ- groups (Paris cohort: P ˂0.0001 for all; BIODEGMAR cohort: P ˂0.05 for all). 5 key findings →
Participants: 212 Evidence: moderate
Full summary, score breakdown and related studies → Original source
N-terminal p-tau was increased in CJD versus SCD (p < 0.0001) and correlated with total tau (t-tau) in the presence of AD and PART co-pathology (rho = 0.758-0.952, p ≤ 001). 5 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood phosphorylated tau (p-tau) biomarkers, including p-tau217, show high associations with Alzheimer's disease (AD) neuropathologic change and clinical stage. 1 key finding →
Participants: 388 Evidence: low
Full summary, score breakdown and related studies → Original source
All assessed BBM levels varied by over 10% by collection tube type. 5 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
p-tau181, NfL, t-tau, and UCHL1 were increased 2- to 4-fold in cirrhosis, whereas GFAP was not increased. 3 key findings →
Participants: 135 Evidence: low
Full summary, score breakdown and related studies → Original source
CSF exhibited increased levels of all SIMOA biomarkers in AD compared to Controls (AUCs: 0.71, 0.86, 0.92, and 0.94, respectively). 4 key findings →
Participants: 43 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Large differences were seen between bvFTD (mean NfL 34.9 pg/mL) and all PPDs and controls (all < 11 pg/mL). 5 key findings →
Participants: 42 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
CSF NPTX2 and serum GFAP levels varied most between diagnostic groups. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
With advances in antiretroviral treatment, the population of older people living with HIV (PLWH) is increasing rapidly, leading to a rise in cognitive impairment related to both HIV and aging. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Higher baseline WMH volume and higher GFAP were associated with a greater likelihood of diagnostic progression. 5 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
Various plasma biomarkers for amyloid-β (Aβ) have shown high predictability of amyloid PET positivity. 1 key finding →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Lower CSF Amyloid beta 1-42 concentrations (p = 0.048), lower Amyloid beta 42/40 ratio (p = 0.038), and higher Tau/Amyloid-beta 1-42 ratio, as well as pTau/Amyloid-beta 1-42 ratio (each p = 0.004) were associated with rpAD. 5 key findings →
Participants: 228 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neurofilament light chain (NfL) is an axonal protein that when measured in cerebrospinal fluid (CSF) serves as a biomarker of neurodegeneration. 3 key findings →
Participants: 278 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The score reflecting the severity of Aβ pathology showed a better correlation with ln(Aβ42/Aβ40) (R 2 = 0.506, β = -0.713, P < 0.001) than with ln(Aβ42) (R 2 = 0.206, β = -0.458, P < 0.001), which was confirmed after adjusting for covariates. 4 key findings →
Participants: 159 Evidence: low
Full summary, score breakdown and related studies → Original source
SerpinA1 (α1-antitrypsin) is a soluble glycoprotein, the cerebrospinal fluid (CSF) isoforms of which showed disease-specific changes in neurodegenerative disorders that are still unexplored in Alz-heimer’s disease (AD). 3 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
We aimed to assess the utility of AT(N) classification in clinical practice. 2 key findings →
Participants: 230 Evidence: low
Full summary, score breakdown and related studies → Original source
This study aimed to investigate the interaction between weight loss (WL) and plasma amyloid-β 42/40 (Aβ 42/40), neurofilament light chain (NfL), progranulin, and their association with cognitive decline over time among older adults. 4 key findings →
Participants: 470 Evidence: low
Full summary, score breakdown and related studies → Original source
Comorbid Alzheimer's disease (AD) neuropathology is common in Lewy body disease (LBD); however, AD comorbidity in the prodromal phase of LBD remains unclear. 2 key findings →
Participants: 84 Evidence: moderate
Full summary, score breakdown and related studies → Original source
AD-MCI and AD-DEM patients showed increased p-tau217 and spectral slowing (higher theta, lower alpha). 4 key findings →
Participants: 128 Evidence: low
Full summary, score breakdown and related studies → Original source
Glial fibrillary acidic protein (GFAP) and neurofilament light (NfL) are putative non-amyloid biomarkers indicative of ongoing inflammatory and neurodegenerative disease processes. 2 key findings →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF irisin correlated positively with BDNF, Aβ42, and MMSE scores, but not with CSF total tau. 2 key findings →
Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 →