Veronica J. Tom, Ph.D.
Assistant Professor, Dept. Neurobiology and Anatomy, Drexel University College of Medicine
Modulation of Extrinsic and Intrinsic Factors to Promote Axonal Regeneration and Plasticity
Research and Interest
There are multiple obstacles to successful axonal regeneration, including a diminished intrinsic growth response from adult axons and the formation of a glial scar around the injury site that is rich with inhibitory matrix molecules. Our goal is to devise strategies that will tackle these different impediments to result in robust axonal regeneration.
Some of the ongoing projects in the lab are:
- Combining transplantation with modification of the inhibitory matrix associated with the glial scar to promote recovery of autonomic function
- Targeting microtubules to enhance the intrinsic axonal regenerative response
- Understanding the role of the transcription factor Sox9 in astrogliosis
B.S., Neural Science, New York University, 1999
Ph.D., Neurosciences, Case Western Reserve University, 2005
Postdoctoral training, University of Arkansas for the Medical Sciences and Drexel University College of Medicine
Tom VJ, Steinmetz MP, Miller JH, Doller CM, Silver J (2004). Studies on the development and behavior of the dystrophic growth cone, the hallmark of regeneration failure, in an in vitro model of the glial scar and after spinal cord injury. J. Neurosci. 24: 6531-6539.
Tom VJ, Doller CM, Malouf AT, Silver J (2004). Astrocyte-associated fibronectin is critical for axonal regeneration in adult white matter. J. Neurosci. 24: 9282-9290.
Steinmetz MP, Horn KP, Tom VJ, Miller JH, Busch SA, Nair D, Silver DJ, Silver J (2005). Chronic enhancement of the intrinsic growth capacity of sensory neurons combined with the degradation of inhibitory proteoglycans allows functional regeneration of sensory axons through the dorsal root entry zone in the mammalian spinal cord. J. Neurosci. 25: 8066-8076.
Houle JD, Tom VJ, Mayes D, Wagoner G, Phillips N, Silver J (2006). Combining an autologous peripheral nervous system "bridge" and matrix modification by chondroitinase allows robust, functional regeneration beyond a hemisection lesion of the adult rat spinal cord. J. Neurosci. 26: 7405-7415.