I am an established electrophysiologist capable of utilizing numerous recording techniques, including dual slice electrophysiology recording with confocal live cell imaging in various types of neurons and glial cells. I am also familiar with various genetic modification and biochemical techniques. For a decade, I have been investigating the role of ion channels and transporters in the interaction/communication among neurons, glia and vasculature to decipher the mechanism of regulation in migration, proliferation and differentiation of neuron and astroglial cells to establish a functional CNS. I have focused on identifying signaling mechanisms between neurons and astrocytes that regulate ion or glutamate homeostasis and subsequently influence excitatory and inhibitory (E/I) balance in the brain. I believe such mechanisms are likely to be involved in the pathology of many CNS disorders, such as neurodevelopmental disorders, autism-associated epilepsy, focal cortical dysplasia and degenerative diseases. Currently, I am interested in amyloid β-peptide (Aβ)-mediated neuronal activity-dependent synaptic alteration and neuro-circuit degeneration in Alzheimer’s disease. Neuronal circuit activities are controlled by Circadian Locomotor Output Cycles Kaput (CLOCK)-mediated activity-dependent protein regulation. My goal is to characterize CLOCK-mediated translational regulation of Aβ precursor (APP) proteins in neurons that regulates specific types of neuro-circuit deterioration which is not only susceptible to Aβ accumulation, but also serves as a conduit for transmitting mutated APP to other cell types in the aging CNS. By exploring Aβ-susceptible neuronal and astrocytic circuit-associated transcriptomes, I hope to identify a unique subset of transcripts, present in specific cell types at specific times and locations, which are involved in the activity-dependent regulation of Aβ-mediated neuronal and glial circuit degeneration. In this way, I hope to uncover novel forms of cross-talk between excitatory and inhibitory synapses and of non-synaptic communication in the aging process. Furthermore, I aim to identify the roles of corresponding activity-dependent proteins in setting the E/I balance in the aging brain. Surprisingly, very little is known regarding CLOCK activity-dependent protein regulation and synaptic alteration in the neuronal circuit developmental process. Even less is known regarding what happens during neurodegenerative processes.