APPsα Rescues Tau-Induced Synaptic Pathology

Abstract

Alzheimer's disease (AD) is histopathologically characterized by Ab plaques and the accumulation of hyperphosphorylated Tau species, the latter also constituting key hallmarks of primary tauopathies. Whereas Ab is produced by amyloidogenic APP processing, APP processing along the competing nonamyloidogenic pathway results in the secretion of neurotrophic and synaptotrophic APPsa. Recently, we demonstrated that APPsa has therapeutic effects in transgenic AD model mice and rescues Ab-dependent impairments.