Acute anti-Aβ antibody exposure induces microglial changes and significantly alters chemokine signaling.

ABSTRACT:

Introduction

While the anti-amyloid-lowering immunotherapies provide the first disease-targeting therapies for the treatment of Alzheimer's disease, there remain harmful adverse events causing hesitation among patients, families, physicians, and regulatory bodies. Though these drugs have been repeatedly proven to lower brain amyloid plaque burden, the specific cellular mechanisms and pathways by which the immunotherapy impacts the brain remain unclear.

Methods

This study aimed to transcriptionally profile the brain's immediate immune response to anti-amyloid beta (anti-Aβ) antibodies. To evaluate acute cellular priorities, we intracranially injected anti-Aβ antibody (3D6) or an isotype-matched control immunoglobulin G (IgG) antibody and performed single-cell sequencing analy

SUBMITTER: Foley KE 

PROVIDER: S-EPMC12789186 | biostudies-literature | 2026 Jan-Mar

REPOSITORIES: biostudies-literature