Enhancement of MerTK expression or function in the brain is likely to increase phagocytosis of all MerTK targets, including myelin, synapses, apoptotic cells and even live neurons in a process termed phagoptosis.77 Bispecific antibodies and hybrid proteins with affinities to both MerTK and amyloid beta have been designed to specifically target amyloid beta to MerTK-mediated, non-inflammatory phagocytosis in Alzheimer’s disease.78,79 Similar strategies could be adopted to selectively enhance α-syn clearance through MerTK in synucleinopathies. Here, MERTK is linked to early-onset autosomal dominant Alzheimer disease.