Local Drug Delivery To Reduce Secondary Injury and Promote Remyelination After Spinal Cord Injury
Thursday, September 1, 2016
10:00 AM-12:00 PM
BIOMED PhD Research Proposal
Title:
Local Drug Delivery To Reduce Secondary Injury and Promote Remyelination After Spinal Cord Injury
Speaker:
Robert Shultz, PhD Candidate, School of Biomedical Engineering, Science and Health Systems
Advisor:
Yinghui Zhong, PhD, Assistant Professor, School of Biomedical Engineering, Science and Health Systems
Abstract:
Spinal cord injury is a debilitating condition that results in severe motor, sensory, and autonomic functional deficit. Following initial mechanical injury, a wave of toxic, inflammatory, and inhibitory molecule expression known as secondary injury causes extensive tissue loss and further functional decline. While some axons persist even through secondary injury progression, secondary injury-associated oligodendrocyte (OL) loss causes widespread demyelination, resulting in poor signal propagation and leaving axons vulnerable to additional insult. Endogenous progenitor populations capable of differentiating into mature, myelinating OLs proliferate in response to injury, but fail to efficiently differentiate, resulting in limited remyelination of denuded axons. Failed progenitor differentiation is attributed to the presence of differentiation-inhibitory signals in the post-injury microenvironment.
We aim to promote functional recovery following SCI by simultaneously attenuating secondary injury progression and directly stimulating OL differentiation. In this study, we will develop and characterize clinically relevant, biomaterials-based drug delivery systems to simultaneously attenuate secondary injury progression and promote OL differentiation to improve functional recovery in a clinically relevant rat contusion model. We hypothesize that targeting both secondary injury and remyelination will reduce inflammation, reduce lesion size, mitigate tissue loss, promote oligogenesis, and enhance myelination of axons, resulting in significantly better functional recovery than either approach alone.
Contact Information
Ken Barbee
215-895-1335
barbee@drexel.edu