27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Blarcamesine, demonstrating a safety profile with no associated neuroimaging adverse events, significantly slowed clinical progression by 36.3% at 48 weeks with blarcamesine group as well as the individual 30 mg (by 34.6%) and 50 mg (by 38.5%) blarcamesine groups vs. placebo on the prespecified primary cognitive endpoint ADAS-Cog13. 5 key findings →
Design: open-label trial Participants: 338 Evidence: high
Full summary, score breakdown and related studies → Original source
Lecanemab treatment resulted in significant reduction in amyloid plaques and a slowing of clinical decline. 5 key findings →
Design: open-label trial Participants: 856 Evidence: high
Full summary, score breakdown and related studies → Original source
Reduction of amyloid via amyloid-targeting therapies may result in clinical benefit. 2 key findings →
Design: clinical trial Participants: 1,582 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In participants with early symptomatic AD, zagotenemab failed to achieve significant slowing of clinical disease progression compared with placebo. 5 key findings →
Design: clinical trial Participants: 360 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Sixty consecutive patients with prodromal or mild AD were screened; 50 were randomized to gamma or sham tACS (mean [SD] age, 67.3 [7.8] years; 25 [50.0%] female and 25 [50.0%] male). 5 key findings →
Design: open-label trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Obicetrapib significantly slowed AD biomarker progression over 12 months in participants with ASCVD, with the greatest effects in ApoE4 carriers. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Mean age of completers (n = 30) was 73.5 years and mean Mini-Mental Status Examination (MMSE) score was 22.5. 3 key findings →
Design: open-label trial Participants: 30 Evidence: high
Full summary, score breakdown and related studies → Original source
Cellular senescence contributes to Alzheimer's disease (AD) pathogenesis. 1 key finding →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source
Despite reductions in plasma p-tau217 with donanemab treatment, this biomarker cannot currently be used to accurately detect TRAC by PET (< 24.1 CL) in individuals with early symptomatic AD. 1 key finding →
Design: phase-3-trial Participants: 830 Evidence: null result
Full summary, score breakdown and related studies → Original source Free full text
Our trial showed that olfactory-stimulated oxygenation differences in the orbitofrontal cortex detected by fNIRS were associated with cognitive impairment and cognitive-related objectives. 5 key findings →
Design: open-label trial Participants: 97 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Gantenerumab reduced amyloid PET load, CSF biomarkers of amyloid beta (Aβ)40, total tau (t-tau), phosphorylated tau 181 (p-tau181), neurogranin, S100 calcium-binding protein B (S100B), neurofilament light (NfL), alpha-synuclein (α-syn), neuronal pentraxin-2 (NPTX2), and plasma biomarkers of t-tau, p-tau181, p-tau217, and glial fibrillary acidic protein (GFAP) while increasing plasma Aβ40, Aβ42. vMRI showed increased reduction in whole brain volume and increased ventricular expansion, while hippocampal volume was unaffected. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Drug development continues robustly at all phases despite setbacks in several programs in the recent past. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The plasma p-tau217 and plasma GFAP models adequately predicted the change over time, with donanemab resulting in decreased plasma p-tau217 and plasma GFAP concentrations. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
BBBO was achieved in 5 out of 6 subjects with an average volume of 983±626 mm 3 following FUS at the right frontal lobe both in white and gray matter regions. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
The concentration of 124 I-RmAb158-scFv8D3, as measured in vivo with PET, increased with age and corresponded well with the ex vivo autoradiography and Aβ immunohistochemistry results. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lecanemab is a humanized IgG1 monoclonal antibody binding with high affinity to protofibrils of amyloid-beta (Aβ) protein. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Part 1 (currently ongoing), between February 6, 2024, and December 27, 2024, 322 adults were screened, of whom 75 (aged 59-89 years) met NIA-AA and IPA criteria. 5 key findings →
Design: clinical trial Participants: 322 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E4 (APOE4) is a major risk factor for Alzheimer’s disease (AD). 4 key findings →
Design: clinical trial Evidence: low
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 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 →