Jon completed a BS at the University of Mount Union in Alliance, Ohio with a double major in Biochemistry and Cognitive and Behavioral Neuroscience. During his undergraduate education, Jon participated in research looking at the beneficial effects of Vitamin E administration and enriched environment on functional recovery following traumatic brain injury under the supervision of Dr. Jeffery Smith. He also studied the neuroprotective effects of nicotine and estrogen against oxidative stress- induced cell death in Alzheimer's Disease, utilizing am in vitro culture system. His fascination with neuroscience and, more specifically, neurodegeneration and injury continued after completion of his undergraduate work. Jon joined the lab of Dr. Sophia Sundararajan as a Research Assistant at ÐÇ¿Õ´«Ã½ in the Department of Neurology and studied the neuroprotective effects and therapeutic aspects of thiozolandinediones for ischemic stroke. This propelled him to pursue science as a career and obtain his Ph.D. Jon started in the graduate program as a direct admit to the Department of Neurosciences at ÐÇ¿Õ´«Ã½. He promptly joined the Zigmond laboratory and set out to answer a question that had been raised by Richard decades earlier. In a 1995 publication from the Zigmond lab, Schereiber et al. showed that macrophages accumulated in the superior cervical ganglion (SCG) after transection of the postganglionic fibers. Richard's question was what role (if any) do these macrophages play in the ganglia and do they perform functions important for peripheral nerve regeneration? Years of research showed that in two mutant murine lines, the Wallerian degeneration slow (WLD) and a C-C chemokine receptor 2 (CCR2) knockout, macrophages did not accumulate in injured dorsal root ganglia (DRG). Using these two murine lines, Jon showed that macrophage accumulation around injured cell bodies was necessary for a maximal regenerative response of those neurons. Following up that research, the lab created an adeno-associated virus to overexpress the macrophage chemokine CCL2 in sensory neurons of the DRG. Data from this project demonstrated that when CCL2 is overexpressed in uninjured DRGs, macrophages accumulate and increase the regenerative capabilities of sensory neurons in a STAT3-dependent manner. In addition to the studying the immune response to peripheral nerve injury, Jon also researched the reduced regenerative capacity of sympathetic and sensory neurons in diabetes. Using a rodent model of type-I diabetes, the lab found that hyperglycemic animals displayed significant deficits in the injury-induced gp130 cytokine signaling pathway which likely contributes to the decrease in axon regeneration observed in diabetes. Jon successfully defended his thesis on July 11th, 2016 and is now a research associate in the lab.