Current Status: Alumni
Graduate Department: Neuroscience
Advisor(s): Jonathan Glass, MD
The Role of Cu,Zn-Superoxide dismutase (SOD1) and Oxidative Stress in the Pathogenesis of Axonal Degeneration
I reported for the first time that loss of the antioxidant protein SOD1 causes a distal motor axonopathy. I went on to show that SOD1 targeted exclusively to the mitochondrial intermembrane space rescues this pathology. This demonstrates that mitochondrial oxidative stress is an important cause of motor axonopathy, and suggests a novel role for mitochondrial SOD1 in the maintenance of motor axons.
During M3-M4 years, I have continued working in my dissertation lab, completing paper submission and revisions. I have also started a new project involving generation of a new transgenic mouse, to be continued by a post-doc in the lab after I move for residency.
Graduation Year: 2011
Residency: Neurology, Johns Hopkins Hospital