28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
CSF biomarkers and amyloid positron emission tomography reflect different aspects of Alzheimer's disease brain pathology, and therefore, less-than-perfect correspondence is expected. 1 key finding →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
In non-demented individuals along the AD continuum, p-tau drives cognitive dysfunction. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
These findings provide additional insight into gut microbial involvement in AD and add to the growing understanding of the gut-brain axis. 2 key findings →
Participants: 410 Evidence: low
Full summary, score breakdown and related studies → Original source
Abeta (1-42/1-40) and GFAP independently associated with amyloid PET status (p = 0.009 and p < 0.001 respectively), and GFAP and NfL independently associated with syndrome diagnosis (p = 0.001 and p = 0.048 respectively). 2 key findings →
Participants: 176 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma NfL levels correlated with disease severity and progression in terms of both motor and cognitive functions in PD. 4 key findings →
Participants: 178 Evidence: low
Full summary, score breakdown and related studies → Original source
Although loss of TAR DNA-binding protein 43 kDa (TDP-43) splicing repression is well documented in postmortem tissues of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), whether this abnormality occurs during early-stage disease remains unresolved. 2 key findings →
Evidence: low
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
Extracellular α-synuclein has been proposed as a crucial mechanism for induction of pathological aggregate formation in previously healthy cells. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Our results suggest that the ki:e SB-C is an objective, scalable, and reliable indicator of cognitive decline, fit for purpose as a remote assessment in clinical early dementia trials. 3 key findings →
Participants: 69 Evidence: low
Full summary, score breakdown and related studies → Original source
Both DELPHI analysis of network function and DTI analysis detected a significant decrease in connectivity, excitability, and WM integrity in the SCD group compared to healthy control (HC) subjects; a significant decrease was also noted for aMCI and Dementia groups compared to HC. 3 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
Understanding the tissue-specific genetic controls of protein levels is essential to uncover mechanisms of post-transcriptional gene regulation. 5 key findings →
Evidence: low
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
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
9 of the 3,322 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 9. The same 9 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 →