Evidence map›Paper›PMID 41981185›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

Anti-amyloid antibody equilibrium binding to Aβ aggregates from human Alzheimer's disease brain.

Katrine D Bjørnholm, P Monroe Butler, Anna E Francis, Curran Varma, Emma T Spooner, Martine B Grenon, Yi Ran Xu, Youqi Tao, Angela L Meunier, Amirah K Anderson and 5 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Katrine D BjørnholmAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0002-6913-1012
P Monroe ButlerAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Anna E FrancisAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Curran VarmaAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Emma T SpoonerAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Martine B GrenonAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID 0009-0008-1113-8466
Yi Ran XuAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Youqi TaoAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Angela L MeunierAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Amirah K AndersonAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Elizabeth L HennesseyDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Michael B MillerDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Dennis J SelkoeAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Cynthia A LemereAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0002-2983-7870
Andrew M SternAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0002-8589-6891

Funding

Mechanisms of Somatic Mutation in Alzheimer's Disease Using Single Neuron AnalysisR01AG082346 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI Michael B Miller · 2024 to 2026
$2.7M
Combination Therapy with Semaglutide and Anti-Amyloid Antibodies for Alzheimers DiseaseR01AG084531 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI CYNTHIA A LEMERE · 2024 to 2026
$2.5M
Understanding and Mitigating Vascular Side-Effects Associated with Anti-Amyloid ImmunotherapyR01NS136122 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI CYNTHIA A LEMERE · 2024 to 2026
$2.5M
Heterogeneity in Toxicity of Oligomeric Amyloid Beta and Neuronal Resilience in Alzheimer DiseaseK08NS128329 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI ANDREW MICHAEL STERN · 2022 to 2026
$1.1M
Genome-Wide Somatic Mutation in Alzheimer's Disease Pathogenesis Using Single Neuron AnalysisK08AG065502 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI MILLER, MICHAEL B · 2020 to 2024
$848k
NIA NIH HHS K08 AG065502NIA NIH HHS R01 AG082346NIA NIH HHS R01 AG084531NIH HHS K08NS128329NIH HHS R01AG082346NIH HHS R01AG084531NIH HHS R01NS136122NINDS NIH HHS K08 NS128329NINDS NIH HHS R01 NS136122
6 · The paper itself

Abstract

introductionLecanemab 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.

methodsEquilibrium binding constants (K

resultsLecanemab 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.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAntibodies, Monoclonal, HumanizedBrainAgedAged, 80 and overAntibodies, MonoclonalApolipoprotein E4Cerebral Amyloid AngiopathyFemaleHumansMalePlaque, AmyloidaducanumabAmyloid beta-PeptidesAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedApolipoprotein E4aducanumabaffinityAlzheimer's diseaseamyloidamyloid‐related imaging abnormalitiesapolipoprotein Ebrain tissuecerebral amyloid angiopathydonanemabfibrilimmunotherapylecanemabprotofibrilsolubility

Identifiers

PMID41981185
PMCPMC13079063

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.