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 cellular pathways for autophagy-lysosome degradation, synaptic vesicle trafficking, neuroinflammation, and protein/lipid kinase signaling in neuropathogenesis.


  • 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.

Autophagy in axons and dendrites


Autophagy implication in axon transport

  • 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.

Autophagy process in mammalian cells        

  • Protein/lipid kinase and phosphatase in regulating synaptic vesicle trafficking and dysfunction in neurotransmission underlying Parkinson’s disease.

LRRK2 protein in 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.

LRRk2 pathophysiology


LRRK2 research program.


  • Genetic animal model development for human movement disorders and neurodegenerative diseases.