27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
hONE-NPCs expressed proteins such as Ki67, Nestin, GFAP, and b-III Tubulin, which are associated with cellular proliferation and the neuronal progenitor lineage. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
As a result of multiple phosphorylation, Tau undergoes early conformational changes involving the bending of the intact amino (N)-terminus over the third repeated domain, which in turn was evidenced by positive immunolabeling with the monoclonal antibody Alz-50 [2]. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Here we present the cases of two individuals with language and behavioral symptoms indicative of the early clinical manifestations of both Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Amyloid immunotherapy with lecanemab and donanemab has been approved on the basis of statistically significant slowing of cognitive and functional decline in early Alzheimer's disease (1,2). 2 key findings →
Design: post-hoc analysis Evidence: low
Full summary, score breakdown and related studies → Original source
A doença de Alzheimer (DA) configura-se como a principal causa de demência em idosos, se tornando um dos maiores desafios da medicina moderna devido à sua alta prevalência e o impacto social associado. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The accumulation of tau proteins in the brain contributes to the therapeutic challenges faced by patients with Alzheimer’s disease, frontotemporal dementia, and other neurodegenerative disorders. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The Phase 2a TOGETHER trial tested bepranemab, an antibody targeting the tau protein (rather than amyloid), in 466 people with prodromal-to-mild Alzheimer's disease over 80 weeks. 3 key findings →
Design: phase-2-trial Participants: 466 Evidence: early
Full summary, score breakdown and related studies → Original source
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
BackgroundTuberous sclerosis complex (TSC) is a rare autosomal dominant neurodevelopmental disorder caused by loss-of-function mutations in TSC1 or TSC2, resulting in chronic hyperactivation of the mechanistic target of rapamycin (mTOR) pathway. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
--Clinical trajectories after a diagnosis of mild cognitive impairment (MCI) vary widely, so prognostic models must account for both the timing of subsequent diagnoses and unequal follow-up. 2 key findings →
Participants: 401 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217 concentrations were positively associated with plasma TNF- (Kendalls {tau} = 0.339; P < .001) and IL-6 (Kendalls {tau} = 0.310; P < .001) concentrations. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
GWAS found associations between plasma biomarkers and the APOE gene. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
9 of the 733 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →