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Find studies

Showing 1–25 of 60 studies matching “lecanemab” scoring ≥ 67 out of 100 (page 1 of 3) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 60 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Lecanemab-related ARIA demonstrates a clear ApoE4 gene-dose effect, supporting routine ApoE4 genotyping before treatment. 3 key findings →

Design: systematic review Participants: 1,576 Evidence: high

1795 participants with early AD were enrolled in Clarity AD, of which 1521 were ApoE ε4 heterozygotes or non-carriers (85 %). 5 key findings →

Design: clinical trial Participants: 1,795 Evidence: high

Compared to placebo, lecanemab demonstrated statistically significant slowing of cognitive decline on CDR-SB and secondary endpoints, including amyloid burden reduction. 3 key findings →

Design: meta-analysis Participants: 698 Evidence: high

The analysis included 8 randomized placebo-controlled trials with 6547 participants. 5 key findings →

Design: meta-analysis Participants: 6,547 Evidence: high

Nineteen randomized placebo-controlled trials with 6918 participants were included. rTMS was significantly more effective than placebo/sham stimulation. 5 key findings →

Design: meta-analysis Participants: 6,918 Evidence: high

BAN2401-G000-201 did not meet the 12-month primary endpoint. 5 key findings →

Design: clinical trial Participants: 18 Evidence: high

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

The FDA approved lecanemab for Alzheimer's disease in January 2023 which acts as a novel disease-modifying anti-amyloid-beta (Aβ) human monoclonal antibody and is administered intravenously. 5 key findings →

Design: systematic review Participants: 2,729 Evidence: high

We report the case of a 79-year-old woman with Alzheimer's disease who participated in a Phase III randomized controlled trial called CLARITY-AD testing the experimental drug lecanemab. 3 key findings →

Design: randomized controlled trial Evidence: high

Four regulatory agencies have approved lecanemab through different pathways, each requiring confirmation of amyloid pathology and careful assessment of ARIA risk, particularly in Apolipoprotein E (ApoE) ε4 homozygotes. 5 key findings →

Design: cohort study Participants: 407 Evidence: moderate

Updated safety results from phase 3 lecanemab study in early Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 78 out of 100. Alzheimer's research & therapy 2024-05-10

Overall, 1795 participants from Core and 1612 participants with at least one dose of lecanemab (Core + OLE) were included. 1 key finding →

Design: open-label trial Participants: 1,795 Evidence: high

Lower baseline C3 was consistently associated with ARIA risk across sensitivity analyses and higher baseline C1q with smaller amyloid reduction at week 26. 4 key findings →

Design: cohort study Participants: 62 Evidence: moderate

In this prospective Korean cohort, lecanemab was generally well tolerated. 3 key findings →

Design: longitudinal study Participants: 127 Evidence: moderate

Compared with an AChEI-based conventional care strategy, lecanemab initiation was associated with comparable treatment persistence and lower observed risks of BPSD, emergency visit as well as reduced use of psychotropic and infection-related medications in exploratory analyses. 5 key findings →

Design: cohort study Participants: 589 Evidence: high

Our analysis found that lecanemab showed significant positive statistical efficacy with respect to cognition, function, and behavior in patients with early AD though the actual clinical significance is yet to be established. 2 key findings →

Design: systematic review Evidence: high

Use of lecanemab for the treatment of Alzheimer's disease: A systematic review

✓ Peer-reviewed alzhub usefulness score 76 out of 100. Brain and behavior 2024-06-01

According to studies, lecanemab lessens clinical deterioration and reduces brain amyloid-beta plaques (difference,.45; 95% confidence interval,.67 to.23; p < .001). 1 key finding →

Design: meta-analysis Evidence: high

Our single-center experience with long-term lecanemab treatment was similar to that observed in clinical trials. 3 key findings →

Design: cohort study Participants: 136 Evidence: high

Lecanemab slowed cognitive decline versus placebo in mild-to-moderate AD by ADCOMS, CDR-SB, and ADAS-Cog. 5 key findings →

Design: systematic review Evidence: high

BackgroundAnti-amyloid monoclonal antibodies offer a treatment strategy for early Alzheimer's disease, but their modest efficacy must be weighed against important safety concerns. 3 key findings →

Design: meta-analysis Evidence: high

These findings support the short-term efficacy and safety of Lecanemab in early AD and highlight plasma biomarkers as a treatment-responsive biomarker. 3 key findings →

Design: cohort study Participants: 68 Evidence: moderate

Plasma p-tau217 levels decreased significantly from 3 months, with the greatest decline between 3 and 6 months, followed by a plateau. 5 key findings →

Design: longitudinal study Participants: 153 Evidence: moderate

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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
  • Randomized / 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
  • Multicenter 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 31,380 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.

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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →

Newest studies, as a dated timeline →    Atom feed    Where this research is being discussed: events