Jill Ward, PhD

(she/her)

Assistant Professor, Department of Cell Biology, School of Medicine

Graduate Programs

Full Member - Genetics and Molecular Biology
Full Member - Neuroscience

Education

Certificate, Emory University, 2022
PhD, University of Louisville, 2012
MS, University of Louisville, 2010
BS, Auburn University, 2007

Contact Information

Email: jill.ward@emory.edu

Phone: 404-727-1808

Address:
Whitehead Biomedical Research Building, Room 545 615 Michael Street Atlanta, GA 30322

Peripheral nerve injuries are common with more than 200,000 new cases reported each year in the United States alone. Only about 10% of these individuals regain much function. There are 17,730 new U.S. spinal cord injuries annually, and the lifetime costs can reach $5 million per person (not including lost wages). Nerve injury and especially spinal cord injury significantly impact long-term quality of life, and most injured individuals seek continued treatments for associated disabilities and pain. The most common explanation for poor functional outcomes is the slow and inefficient process of axon regeneration. Enhancing axon regeneration is a primary therapeutic target for the improvement and restoration of function after nervous system injuries, such as spinal cord and peripheral nerve injuries. Axons in peripheral nerves have a limited ability to regenerate, whereas axons in the central nervous system exhibit extremely little regeneration. Our overall goal is to understand mechanisms that limit or enhance regeneration in pursuit of promoting functional recovery after neural injuries. Towards this overall goal, I have two current interests: 1) plasticity of the sympathetic nervous system at neuromuscular junctions and 2) role of sympathetic innervation and motor performance.

Sympathetic plasticity. Axons within the spinal cord and nerve consist of motor, sensory, and sympathetic axons, which undergo plasticity after injury. A critical knowledge gap in neuroscience is understanding the purpose of sympathetic axon terminals within the neuromuscular synapse, how sympathetic axons associated with neuromuscular junctions respond to neural injuries, and what their contribution is to functional recovery or dysfunction. Preliminary evidence suggests that the sympathetic innervation of neuromuscular junctions can modulate mitochondrial respiration and biogenesis, synaptic stability, and muscle strength as well as control the muscle response to exercise and activity. The goals of our newest work will test the hypothesis that sympathetic neurons are required for the functional and metabolic stability of the neuromuscular unit in normal and pathological conditions.

My research program sits at the interphase of fundamental biology and translational biology. While the prospects of impact in nerve injury and regeneration are clear, my study of muscle metabolic adaptations controlled by the sympathetic system go well beyond nerve injury. I suspect that the muscle mitochondrial biology we will discover will further impact other prevalent diseases, such as aging-dependent sarcopenia and metabolic syndrome. The current research directions dove-tail nicely with my long-standing interests in enhancing axon regeneration with neuronal activity, including exercise, electrical stimulation, and optogenetic approaches. My Department of Cell Biology offers a propitious environment to expand the fundamental cell biology of the muscle with an eye in translation.