Evidence map›Paper›PMID 40475543›Full record

ArticlebioRxiv : the preprint server for biology2025

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

P Monroe Butler, Anna Francis, Angela L Meunier, Amirah K Anderson, Elizabeth L Hennessey, Michael B Miller, Cynthia A Lemere, Dennis J Selkoe, Andrew M Stern

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

P Monroe ButlerAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Anna FrancisAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Angela L MeunierAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Amirah K AndersonAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Elizabeth L HennesseyDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Michael B MillerDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Cynthia A LemereAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Dennis J SelkoeAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Andrew M SternAnn Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.ORCID 0000-0002-8589-6891

Funding

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
NINDS NIH HHS K08 NS128329NINDS NIH HHS R01 NS136122
6 · The paper itself

Abstract

Importance: Anti-amyloid immunotherapy is used to treat Alzheimer disease (AD) with moderate benefits and potentially serious side effects due to amyloid related imaging abnormality with effusions/edema (ARIA-E). Different anti-amyloid antibodies have different Objectives: To determine whether anti-amyloid antibodies bind different species of human brain Aβ and whether these binding properties to human brain Aβ explains ARIA-E rates. Design: Cross-sectional study of 18 postmortem human brains. Setting: Single tertiary care hospital. Participants: Deceased patients with AD and cerebral amyloid angiopathy (CAA). Main Outcomes and Measures: Equilibrium binding constants (K Results: Lecanemab did not bind with greater affinity to the soluble fraction of Aβ compared to aducanumab. All three antibodies were bound essentially identical quantities of Aβ across the 18 cases and fractions (Pearson's r 0.84 - 0.97). Antibody preference for plaque Conclusions and Relevance: The lecanemab binding target in human brain is unlikely to be distinctly "protofibrillar" compared to other antibodies. Differences in antibody preference for plaque

Identifiers

PMID40475543
PMCPMC12139811

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Registered trials

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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.