Validation was conducted across 94 households over 365 nights, totalling 297,297 monitoring hours. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Validation was conducted across 94 households over 365 nights, totalling 297,297 monitoring hours. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tau protein misfolding and deposition in the brain is a common factor across many neurodegenerative diseases, grouped under the term tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) levels in the cerebrospinal fluid (CSF) have been associated with Alzheimer disease (AD) status. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Autosomal dominant Alzheimer disease (ADAD) is caused by pathogenic variants in the APP, PSEN1 and PSEN2 genes, but a substantial fraction of reported variants is of unknown clinical significance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217. 4 key findings →
Participants: 484 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Dementia Trials Accelerator (DTA) is a UK-wide programme designed to improve the feasibility, efficiency, and inclusiveness of recruitment into clinical trials of dementia and related brain-health conditions. 5 key findings →
Participants: 10,000 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BACKGROUNDQuantitative amyloid-beta (A{beta})-PET is increasingly used in AD prevention trials. 3 key findings →
Design: longitudinal study Participants: 433 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
BackgroundThe brain age gap (BAG), the difference between neuroimaging-predicted and chronological age, captures inter-individual variation in brain aging. 2 key findings →
Design: longitudinal study Participants: 202 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
INTRODUCTIONBiomarkers for monitoring disease activity and treatment response in peripheral neuropathies remain limited. 3 key findings →
Participants: 81 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundPlasma phosphorylated tau at threonine 217 (p-Tau217) is a leading blood-based biomarker for Alzheimers disease (AD). 1 key finding →
Participants: 449 Evidence: moderate
Full summary, score breakdown and related studies → Original source
BackgroundClonal haematopoiesis (CH), the age-related expansion of mutated blood stem cells, is detectable in around 10% of people in their seventies, rises steeply with age, and is associated with several diseases. 5 key findings →
Design: longitudinal study Participants: 1,091 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma biomarkers of amyloid-associated tau phosphorylation (T1) and established tau proteinopathy (T2) can approximate Alzheimers disease stage, but whether plasma-defined stages correspond to broader biological states is unknown. 1 key finding →
Design: cross-sectional Participants: 1,035 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We focus on neuroinflammation in disorders associated with frontotemporal lobar degeneration (FTLD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cellular mechanisms in early Alzheimers disease (AD) remain poorly understood despite generation of extensive observational multiomic data. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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 →