Toward inflammation-free therapeutics in Alzheimer's disease

Abstract

An engineered fusion protein exploits the efferocytosis pathway to clear amyloid-beta (A beta) from the brain without eliciting the severe inflammatory adverse effects associated with A beta-targeting antibody-based immunotherapies. In mouse models of Alzheimer's disease, this approach induced robust clearance of A beta without inflammation, improved synapse protection, and decreased brain microhemorrhage, which result in superior behavioral recovery.