ADAM10, a major alpha-secretase involved in amyloid precursor protein sheddling, limits beta-amyloid formation by controlling trafficking from dendritic Golgi outposts to synaptic membranes and is thus an integral factor of ADAM10 activity; increasing its activity via synaptic trafficking regulation could provide an effective treatment strategy against Alzheimer’s disease [143,144,145]. This evidence concerns the gene ADAM10 and early-onset autosomal dominant Alzheimer disease.