The molecular mechanisms regulating the normal function of the Amyloid Precursor Protein (APP) has largely remained elusive despite its central role in the pathogenesis of Alzheimer’s disease. Previously, I identified the GABA type B receptor subunit 1a (GABABR1a) as a synaptic receptor for the shed APP ectodomain (sAPP) and revealed a physiological role for sAPP in regulating GABABR1a function to modulate synaptic transmission.

Current work of the lab is aimed at further dissecting the role of APP in specific cell types of the brain and determining the consequences of this signaling on multiple pathways including neurodevelopment, inflammation, myelination and mitochondrial function. The lab aims to exploit this normal function of APP to counteract disease processes and develop novel strategies for the treatment of Alzheimer’s disease.

My Publications