My research focuses on the mechanisms and function of autophagy in manganese (Mn)-induced neurotoxicity. Chronic exposure to high levels of Mn results in an extrapyramidal disorder resembling Parkinsonâ€™s disease. At the cellular level, Mn impairs mitochondrial respiration, leading to energy failure and generation of reactive oxygen species (ROS). The autophagy-lysosome pathway is an essential component of intracellular degradation and quality control, and confers cytoprotection against neurodegeneration by timely removal of dysfunctional mitochondria. It is widely accepted that autophagic dysfunction contributes to pathogenesis of various neurodegenerative disorders, but the role of autophagy in Mn-induced neurotoxicity has yet to be established. The underlying hypothesis of my study is that compromised autophagy contributes to the pathogenesis of Mn neurotoxicity. It is anticipated that the study will provide novel information about cellular and molecular mechanisms underlying Mn-induced neuropathology and identify mechanistic-based therapeutic strategies for the treatment of neurologic deficits.