|
Trained in neuroscience and neuroanatomy, Dr. Gary oversees research in the laboratory in the International Center for Spinal Cord Injury at Kennedy Krieger Institute.
Biographical Sketch:
Dr. Devin Gary received his Ph.D. in 2002 from the University of Kentucky after dual training at UK and the National Institute on Aging at Johns Hopkins Bayview Campus under the direction of Dr. Mark Mattson. After three years post-doctoral training in the Department of Neuropathology at Johns Hopkins with Dr. David Borchelt, Dr. Gary joined the International Center for Spinal Cord Injury at Kennedy Krieger Institute as a Faculty Instructor to work with Dr. John McDonald. Dr. Gary currently oversees research on spinal cord injury in the ICSCI laboratory.
Research Summary:
Traumatic spinal cord injury (SCI) is a devastating condition resulting in cell death of neural tissue, interruption of ascending and descending tracts and loss of myelin. The use of transplanted cells to reduce or replace cell loss (i.e. neurons and glia) in the spinal cord is a major focus of current research in the SCI field. Emphasis in this area has been placed on the use of cells to deliver trophic support to tissue (e.g. growth factor expression), the use of neuronal progenitors to replace lost motor or sensory function and the use of oligodendrocyte progenitors to replace myelin.
While it is likely that some combination of all these approaches may be needed to achieve a true therapeutic tool in cell transplantation therapy, we still know very little about the impact of the injured cord’s environment on the transplanted cells’ survival, differentiation or integration. In addition, how transplanted cells actually promote recovery of function following SCI is still an open area of investigation.
Dr. Gary’s research involves approaches aimed at understanding the mechanisms and role of remyelination following spinal cord injury. This work focuses on remyelination from both endogenous oligodendrocyte progenitor cells and transplanted embryonic stem (ES) cell-derived oligodendrocytes. Previous research suggests that functional remyelination, even in modest amounts, can translate into tremendous gain of function following spinal cord injury. Using mouse ES cells as a tool, Dr. Gary is addressing the best ways to achieve remyelination following spinal cord injury.
Recent Publications/Presentations:
RNA interference as a potential therapy for Huntington’s Disease. The Huntington’s Disease Society for America Coalition for the Cure annual meeting. Cleveland, OH, September, 2004.
Gary D.S., Milhavet O., Camandola S., Mattson M.P. (2003) Essential role for integrin linked kinase in Akt-mediated integrin survival signaling in hippocampal neurons. Journal of Neurochemistry, 84, 878-90.
Gary D.S., Mattson M.P. (2002) PTEN regulates Akt kinase activity in hippocampal neurons and increases their sensitivity to glutamate and apoptosis. Neuromolecular Medicine, 2, 261-9.
Milhavet O., Martindale J., Camandola S., Chan S.L., Gary D.S., Cheng A, Holbrook N.J., Mattson M.P. (2002) Involvement of Gadd153 in the pathogenic action of presenilin-1 mutations. Journal of Neurochemistry, 83, 673-81.
Conant K., Haughey N., Nath A., St. Hillaire C., Gary D.S., Pardo C.A., Wahl L.M., Bilak M., Milward E., Mattson M.P. (2002) Matrix metalloproteinase-1 activates a pertussis toxin-sensitive signaling pathway that stimulates the release of matrix metalloproteinase-9. Journal of Neurochemistry, 82, 885-93. | 