My research interest is to understand the cellular and molecular mechanisms underlying cell-cell communications (secreting factors, synapses…) in the brain, and roles of these communications in brain function and pathophysiology of autism and metabolic disorders. To date, my research has revealed that: 1) hypothalamic astrocytes secret TGF-β to induce neuroinflammation and peripheral metabolic disorders; 2) hypothalamus stem cells control brain function and aging though secreting extracellular vesicles (exosomes); 3) autophagy in hippocampal neurons regulates synaptic plasticity and cognitive deficits in autism.

Autism spectrum disorders (ASDs) is a group of developmental disorders. In 2020, approximately 1 in 54 children in the U.S. is diagnosed with autism, according to the Centers for Disease Control and Prevention (CDC). Fragile X syndrome (FXS) is the leading genetic cause of autism and the most common form of heritable intellectual disabilities.  The prevalence of Fragile X syndrome is estimated as 1 in 3,000 in males and as 1 in 6,000 in females. Patients with autism exhibit complex and debilitating neurological phenotypes, including impaired cognition, hyperactivity to sensory stimuli, and social deficits. Effective treatment for ASDs and Fragile X syndrome is still lacking.

Currently, our research is focused on investigating how autophagy and exosomes regulate brain synaptic transmission and neural circuits controlling sensory, cognition, and behaviors. Findings from our research are expected to develop novel therapeutic strategies for cognitive and social deficits associated with autism spectrum disorders.