Harvard Catalyst Profiles

Alzheimer's disease (AD) is the most common neurodegenerative disease, and mutations in Presenilins and Amyloid Precursor Proteins (APP) have been linked to familial forms of AD. Over the past decade, I have been deeply involved in AD research, contributing significantly to our understanding of synaptic dysfunction and mitochondrial calcium dysregulation in AD pathogenesis. As an expert electrophysiologist in the field of neurophysiology, I have also developed a comprehensive understanding of mouse genetics and have acquired expertise in behavioral paradigms for assessing learning and memory in AD mouse models. My work has focused on the physiological roles of gamma-secretase and APP in the adult mouse brain, particularly within the hippocampal network, highlighting their crucial roles in synaptic plasticity at hippocampal synapses. Since 2023, I have broadened my research interests to include the regulation of ion channels in chronic pain and the exploration of synaptic dysfunction in amyotrophic lateral sclerosis and frontotemporal dementia.