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Lecanemab Therapy and APOE Genotype
Kane M.. NCBI Bookshelf, Bethesda (MD), 2024-11-25
Topic: Brain proteins, microglia and lab models
Lecanemab, brand name Leqembi, is a monoclonal antibody that targets amyloid beta (Aβ) aggregates for the treatment of Alzheimer disease (AD) (1). It is approved by the US Food and Drug Administration (FDA) for individuals with mild cognitive impairment (MCI) or mild dementia stage AD with confirmed amyloid pathology (1). Tests to confirm Aβ pathology in the clinical trials included positron emission tomography (PET) or cerebrospinal fluid (CSF) measurement of the Aβ42/Total Tau ratio (2). This disease-modifying medication is based on the amyloid cascade hypothesis, which suggests Aβ aggregates are a key driver in AD pathogenesis and that the removal of Aβ aggregates should slow cognitive decline. Lecanemab is associated with amyloid-related imaging abnormalities (ARIA) due to edema (ARIA-E) or hemorrhage (ARIA-H) from blood vessels in the brain (3, 4). Individuals who have one or 2 copies of the AD risk-associated apolipoprotein E (APOE) ε4 (NM_000041.4:c.388T>C) allele have an increased risk of ARIA-E or -H (1) (Table 1). These individuals require additional monitoring during the first year of treatment (5). The FDA-approved label reports that concomitant antithrombotic medication (aspirin, antiplatelet, or anticoagulant) with lecanemab therapy resulted in intracerebral hemorrhage in 2.5% of individuals during clinical trials (1). The appropriate use recommendations from the Alzheimer’s Disease and Related Disorders Therapeutics Work Group state that individuals requiring anticoagulants should not be treated with lecanemab until additional data regarding this interaction are available (5). Both the FDA-approved label and Alzheimer’s Disease and Related Disorders Therapeutics Work group encourage clinicians to consider participation in a registry for AD treatment to gather additional real-world data on lecanemab therapy (1, 5). [Table: see text]
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Kane, M. (2026). Lecanemab Therapy and APOE Genotype. NCBI Bookshelf, Bethesda (MD).
Vancouver
Kane M. Lecanemab Therapy and APOE Genotype. NCBI Bookshelf, Bethesda (MD). 2026. PMID: 39141762.
BibTeX
@article{kane2026-39141762,
author = {Kane, M.},
title = {{Lecanemab Therapy and APOE Genotype}},
journal = {NCBI Bookshelf, Bethesda (MD)},
year = {2026},
pmid = {39141762}
}
Built from the record alzhub holds for this paper, not looked up. This record has no DOI, so the citation leaves it out. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Lecanemab is associated with amyloid-related imaging abnormalities (ARIA) due to edema (ARIA-E) or hemorrhage (ARIA-H) from blood vessels in the brain (3, 4).
- Individuals who have one or 2 copies of the AD risk-associated apolipoprotein E (APOE) ε4 (NM_000041.4:c.388T>C) allele have an increased risk of ARIA-E or -H (1) (Table 1).
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Study details
- Effect size2.5%
- Evidence strengthLow
How this study scored 50/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, studied in people and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 29 of the 58 points we could judge it on, which is 50 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (NCBI Bookshelf, Bethesda (MD)) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 5 / 5 | 2026 — within 1 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 2 / 3 | Effect reported as a number, without an interval or test |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 39141762) |
| Free to read | 2 / 2 | Free to read |
| Points | 29 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 29 of the 58 points we could judge it on is 50 out of 100. |
| Total | 50 / 100 | — |
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