Overview
- Washington University researchers reprogrammed astrocytes with chimeric antigen receptors to recognize and engulf amyloid-β in mouse brains.
- An early, single injection prevented plaque formation in genetically prone young mice by the age when brains are typically saturated with amyloid.
- In older mice already carrying plaques, the therapy cut amyloid burden by roughly 50% three months after treatment compared with controls.
- A single AAV dose sustained CAR expression in astrocytes for at least three months and triggered a coordinated astrocyte–microglia response.
- Commentary in Science notes potential advantages over repeated anti-amyloid antibodies and platform flexibility, while emphasizing delivery and safety hurdles before translation.