Molecular, Cellular, Behavioral Biology and

Translational Research in Neurodegeneration

Our long-term goal is to understand the molecular and cellular mechanisms of neurodegeneration that causes human neurological disorders such as Parkinson’s, Huntington’s and Alzheimer’s diseases. Our mission is to translate our knowledge from basic research to the development of molecular diagnostics and therapeutics for neurological disorders. Our primary research interests encompass molecular and cellularpathways for autophagy-lysosome degradation, synaptic vesicle trafficking, neuroinflammation, and protein/lipid kinase signaling in neuropathogenesis.

Autophagy-lysosome pathways

Autophagy-lysosome pathway as neuroprotection mechanism in the maintenance of axon and dendrite homeostasis and the clearance of protein aggregates, including polyQ expansion proteins (such as Huntingtin), tau and alpha-synuclein. The regulation of autophagy and endocytosis in neurons and neurodegeneration by PI3K-III lipid kinase complex proteins, including the modulators/adaptors: Beclin 1, Atg14L, URRAG, Rubicon and NRBF2; development of small compounds as modulators for PI3K-III activity and neuronal autophagy.

 LRRK2 protein in Parkinson’s disease

Protein/lipid kinase and phosphatase in regulating synaptic vesicle trafficking and dysfunction in neurotransmission underlying Parkinson’s disease. The contribution of peripheral immune system and CNS glial cells to the neuroinflammation pathways underlying neurodegeneration mechanism in Parkinson’s disease and other human disorders.