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Anti-amyloid antibody equilibrium binding to Aβ aggregates from human Alzheimer's disease brain
Bjørnholm KD, Butler PM, Francis AE, Varma C, Spooner ET, Grenon MB, Xu YR, Tao Y et al.. Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026-04-01
Topic: Amyloid, tau and blood-test diagnosis
Introduction Lecanemab binds "protofibrils," which are poorly characterized in human brain. It is unknown why lecanemab caused fewer amyloid-related imaging abnormalities (ARIAs) than other antibodies in trials. The apolipoprotein E (APOE) ε4 allele increases ARIA risk through unknown mechanisms. Methods Equilibrium binding constants (K D ) and total amyloid beta (Aβ) binding (B max ) of aducanumab, lecanemab, and donanemab equivalents to soluble and insoluble amyloid plaque-enriched and cerebral amyloid angiopathy (CAA)-enriched Aβ were compared across 17 Alzheimer's disease (AD) cases by mixed models. Titrated immunofluorescence (IF) staining compared antibody binding. Results Lecanemab and aducanumab had indistinguishable preference for "protofibrils." Antibody preference for plaque-enriched versus CAA-enriched Aβ did not differ in soluble extracts or by IF staining but differed slightly in insoluble extracts. The APOE ε4 allele was associated with more soluble antibody-accessible Aβ. Discussion Lecanemab's binding target is similar to other antibodies'. Differences in antibody preference for plaque versus CAA Aβ may not explain differences in ARIA with edema rates.
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APA 7th
Bjørnholm, K. D., Butler, P. M., Francis, A. E., Varma, C., Spooner, E. T., Grenon, M. B., et al. (2026). Anti-amyloid antibody equilibrium binding to Aβ aggregates from human Alzheimer's disease brain. Alzheimer's & dementia : the journal of the Alzheimer's Association. https://doi.org/10.1002/alz.71350
Vancouver
Bjørnholm KD, Butler PM, Francis AE, Varma C, Spooner ET, Grenon MB, et al. Anti-amyloid antibody equilibrium binding to Aβ aggregates from human Alzheimer's disease brain. Alzheimer's & dementia : the journal of the Alzheimer's Association. 2026. doi:10.1002/alz.71350. PMID: 41981185.
BibTeX
@article{bjornholm2026-41981185,
author = {Bjørnholm, K. D. and Butler, P. M. and Francis, A. E. and Varma, C. and Spooner, E. T. and Grenon, M. B. and Xu, Y. R. and Tao, Y. and others},
title = {{Anti-amyloid antibody equilibrium binding to Aβ aggregates from human Alzheimer's disease brain}},
journal = {Alzheimer's \& dementia : the journal of the Alzheimer's Association},
year = {2026},
doi = {10.1002/alz.71350},
pmid = {41981185},
url = {https://doi.org/10.1002/alz.71350}
}
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Key findings
- Results Lecanemab and aducanumab had indistinguishable preference for "protofibrils." Antibody preference for plaque-enriched versus CAA-enriched Aβ did not differ in soluble extracts or by IF staining but differed slightly in insoluble extracts.
- The APOE ε4 allele was associated with more soluble antibody-accessible Aβ.
- Differences in antibody preference for plaque versus CAA Aβ may not explain differences in ARIA with edema rates.
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Study details
- Evidence strengthLow
How this study scored 50/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, 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 | 9 / 10 | Tier 2 — leading specialty journal (Alzheimer's & dementia : the journal of the Alzheimer's Association) |
| 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 | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| 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 41981185) |
| 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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