To decipher the cellular and molecular mechanism of ocular neurodegeneration processes, to develop and test therapeutic strategies and to establish molecular genetic diagnosis of inherited retinal dystrophies are the major research goals in our lab. We investigate the pathophysiology and genetic profiles in retinal degenerations and relate the findings in human patients to those in animal models with homologous genetic defect. As recent advances in therapeutic research (particular gene therapy or human inducible pluripotent stem cell (iPS) therapy), our research is focused on evaluating the therapeutic success by short- and long-term follow-up in animal models, developing the optimized biomarkers and application procedures for future clinical trials.
Retinitis pigmentosa (RP), a heterogeneous group of diseases with variable clinical manifestations, affects approximately 1 in 4,000 people worldwide. The dilemma in understanding RP is the question of how so many different and diverse primary genetic lesions causes the same clinical manifestation that characterizes RP. Information gained from the next generation sequencing-based genetic screening will directly aid in patients’ diagnosis, prognosis and treatment.
We are interesting in investigating the different effects of neuroprotectants in animal disease model of optic neuropathies---the optic nerve crush model and rodent anterior ischemic optic neuropathy model. Our main goal is to study the pathophysiology of RGCs death in axon injury and to evaluate the neuroprotective mechanisms of potential therapeutic agents for optic neuropathies.
Autophagy is an intracellular self-degradative process to maintain cellular metabolism and homeostasis. Increasing studies have implicating deregulation of autophagy has been implicated in the pathogenesis of several ocular diseases, such as age-related macular degeneration, glaucoma, diabetic retinopathy. Our long-term goal is to study the function of autophagy in prevention of neuron cell damage and manipulate autophagy as a treatment against ocular neurodegeneration.