The central goal of this project is to understand how mutations in synaptic chaperone CSPα, which cause Adult onset neuronal ceroid lipofuscinosis (ANCL), disrupt the function of CSPα in stabilizing the SNARE-protein SNAP-23; and how destabilization of SNAP-23 disrupts lysosomal pathology of ANCL. We also propose to rescue these defects using specific chemical chaperones.