Crocker, who joined the UConn Health Center’s research team in November 2007, will also be conducting a restorative study focusing on oligodendrocytes, the cells in the brain responsible for producing myelin. He received a three-year, $530,000 grant for his project entitled, “TIMP-1 Regulation of Oligodendrocyte Differentiation for CNS Remyelination.” The ability of oligodendrocytes to make myelin is enhanced by the protein TIMP-1, which is made by another type of cell in the brain called an astrocyte. One idea about what goes wrong in MS is that astrocytes stop making TIMP-1. Because the astrocytes in people with MS do not produce TIMP-1 they can no longer stimulate myelin to form; thus, when damage is done to the myelin, no repair occurs. “My study focuses on TIMP-1, a protein that enhances the oligodendrocytes ability to make new myelin,” said Crocker, who has also received from the National MS Society the National Multiple Sclerosis Society Career Transition Award and the Dale McFarlin Travel Award for post-doctoral fellows. “The interesting thing is that people with MS do not make this protein. We want to understand how TIMP-1 helps the oligodendrocytes make and become able to produce new myelin. We also want to know if a person with MS did have TIMP-1, would that alone be enough to repair the myelin damaged by multiple sclerosis?” When Crocker first started working on TIMP-1 as a post-doctoral researcher, he received an advanced postdoctoral fellowship from the National MS Society while at the Scripps Research Institute, located in La Jolla, Cal. His project entitled, “Molecular Regulation Of TIMP-1 Gene Expression And Its Role In CNS Inflammation,” focused on understanding
molecular signals that may help to control active players in the inflammation process that occurs in MS-like disease in mice. Since the beginning of that study in 2003, he has continually expanded upon his TIMP-1 research. “If my new study is able to determine that the TIMP-1 protein alone is sufficient to repair damaged myelin, restoration of this protein to the lesions could reverse the damage of MS,” said Crocker, hopefully. “We will also be looking for ways to create something that could also mimic how TIMP-1 can stimulate brain repair.” Research related to restoring function lost in MS, a key priority in the National MS Society’s comprehensive research campaign, focuses on understanding how nerves and their protective myelin coating work normally and how repair of these critical tissues and cells can be facilitated. Results from these studies and other restorative research projects are expected to suggest new ways to repair damage to the nervous system with the hope of improving function for those living with MS. Significant research progress occurred over the course of 2013, offering new leads that are driving efforts to stop MS in its tracks, restore function, and end MS forever. Researchers now have a better idea of what’s causing MS damage and progression, understand more than ever the benefits of early and continuous treatment, and know more about what factors influence the body’s brain repair mechanisms. For more information on local, national and international MS research projects funded by the National MS Society, please visit www.nationalMSsociety.org.
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