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
Research
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
50/100
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
A group of living former NFL players with cognitive and neuropsychiatric symptoms had higher tau levels measured by PET than controls in brain regions that are affected by CTE and did not have elevated amyloid-beta levels. 2 key findings →
Participants: 26 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
Overall, the results suggest that ARC is reliable and valid and represents a feasible tool for assessing cognitive changes associated with the earliest stages of AD. 4 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
Middle-aged adults at risk of dementia show evidence of poorer cognitive performance, principally in visuospatial functions. 1 key finding →
Participants: 210 Evidence: low
Full summary, score breakdown and related studies → Original source
Repeated smartphone-assisted cognitive testing is feasible with reasonable adherence and moderate relative validity for the Stroop and the Trail Making tests compared with conventional neuropsychological tests. 3 key findings →
Participants: 151 Evidence: low
Full summary, score breakdown and related studies → Original source
Detecting early signs of cognitive decline is crucial for early detection and treatment of Alzheimer's Disease. 3 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
We found patient and care partner input to be critical throughout the development process for early identification of design and usability issues and for identifying solutions not previously considered by our research team. 2 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
BrainCheck was able to distinguish between diagnoses of dementia, MCI, and NC, providing a potentially reliable tool for early detection of cognitive impairment. 1 key finding →
Participants: 99 Evidence: low
Full summary, score breakdown and related studies → Original source
Although there were no significant changes in caregiver burden, we were encouraged by the increased emotional well-being of our participants following the completion of our program. 4 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
Web-based cognitive tests have potential for standardized screening in neurodegenerative disorders. 3 key findings →
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
First, in the normative sample, the total score on the Inbrain CST was significantly affected by age, years of education, and gender. 4 key findings →
Participants: 480 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
Several genetic risk factors for Alzheimer's disease implicate genes involved in lipid metabolism and many of these lipid genes are highly expressed in glial cells 1 . 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 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.
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 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 →