Anti-amyloid antibody therapies for Alzheimer's disease: how much do we really understand?

Abstract

A new study published inNature Neurosciencedemonstrated that Fc effector function is essential for amyloid aggregate clearance during lecanemab treatment, a recently FDA-approved therapy for Alzheimer's disease. These findings underscore the requirement for intact Fc-mediated activity to achieve therapeutic efficacy. In addition, single-cell RNA sequencing identified microglia transcriptomic changes that are unique to lecanemab treatment and extend beyond previously characterized microglial activation signatures. Together with a retrospective review of anti-amyloid antibody development and related mechanisms, this commentary provides important insights into new directions for the design of next-generation therapies for Alzheimer's disease.

Keywords

Lecanemab / Alzheimer's disease / Amyloid-β / Therapeutic target / Microglia

Ethical statements

Not applicable.

Author contributions

The author confirms sole responsibility for the following: conception and design, data collection, analysis and interpretation of results, and manuscript preparation.

Data availability

Data sharing not applicable to this article as no datasets were generated or analyzed during the current commentary.

Conflict of interest

The author declares that there is no conflict of interest.

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