Clearance of damaged mitochondria, termed mitophagy, is dysregulated and thereby lead to accumulation of damaged mitochondria and synaptic deficits in neurons. However, the underlying mechanisms for mitochondrial dysfunction and mitophagy deficits remains elusive. We are currently studying the role of mitochondria and mitophagy in the pathogenesis of Alzheimer's disease as well as aging.

In parallel, we are advancing drug discovery efforts through the development of a high-throughput screening platforms based on cellular models of tau and α-synuclein aggregation—key pathological hallmarks of Alzheimer's disease and Parkinson's disease respectively. These platforms enable systematic screening of diverse compound libraries, including kinase inhibitors, FDA-approved drugs, and CNS-penetrant molecules. By integrating these approaches, our work aims to uncover previously unrecognized molecular mechanisms and to identify therapeutically relevant compounds with the potential for clinical translation. 

Research Focus

• Molecular and cellular pathology of Alzheimer’s disease

• Pathogenic role of lipid metabolism in Alzheimer’s disease 

• Pathogenic mechanisms of tau aggregation and propagation

• Mitochondrial dysfunction in neurodegenerative disease

• Development of the novel therapeutic intervention for neurodegenerative diseases