Alexander Gow, Ph.D., a professor at the Wayne State University School of Medicine, has just been awarded a research grant by the National Multiple Sclerosis Society to fund his exploration of a novel model of MS pathology. Gow is a holder of the Charles H. Gershenson Distinguished Fellow Professor title, and is also associate director of the WSU Center for Molecular Medicine and Genetics. He will be using the 3-year, $663,959 funding for his study titled, “Neurodegeneration associated with metabolic stress in oligodendrocytes.”
According to Gow, MS’s early to mid phases exhibit clinical signs rooted in significant brain damage, observed as autoimmune lesions, white and grey matter atrophy, and cognitive impairment. A great number of studies have only been concerned with discovering and developing ways to address the disease’s autoimmune aspect. The largely unmet need to address MS’ cognitive deficits has been for the most part ignored.
Gow shares that over the past few years, researchers have managed to arrive at a number of significant findings on MS, including the discovery that potent and long-term immunosuppression is only modestly able to retard disease progression, and does nothing to keep cortical brain damage in check.
“In this study, we tackle both of these issues using a new model of MS pathology that does not involve autoimmune stimulation to generate disease symptoms,” said Gow. “Rather, we activate metabolic stress in oligodendrocytes to cause dysfunction and death of these cells, which is a potential disease mechanism that has gained experimental support from several laboratories.”
Through this new funding, Gow will be working on establishing a new animal model that may better explain MS pathology, and hopefully bridge the knowledge gap in how MS affects behavioral change and cognitive function. His work will also be testing a treatment formulated to preserve these oligodendrocytes and neurons from degeneration caused by primary metabolic stress.
“There is increasing evidence,” Dr. Gow said, “To indicate that autoimmune attacks on the central nervous system may be a secondary event rather than the primary cause of MS. This indicates that researchers must cast a broader net to test new ideas and develop alternative models that could shed fresh light on MS etiology.”
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