Clinical Neurosciences Center Researchers Awarded $5.7 Million in Grants

Clinical Neurosciences Center Researchers Awarded $5.7 Million in Grants

Oct 9, 2008 2:59 PM

University of Utah Clinical Neurosciences Center researchers have been awarded $5.7 million in grants to study neurodegenerative diseases and disorders that progressively and irreversibly leave people physically and mentally disabled, cause foot ulcers that can lead to amputation, and influence tumor growth.

   • Stefan M. Pulst, M.D., professor and chair of neurology in the School of Medicine, received $1.8 million from the National Institutes of Health (NIH) to continue his longstanding research on degenerative ataxias and the role of ion channels and Parkinson disease-related proteins in neurodegenerative disease.

   • Gordon Smith, M.D., and J. Robinson Singleton, M.D., both associate professors of Neurology, have received a $588,000 grant from the American Diabetes Association (ADA) and a $1.9 million NIH grant to study neuropathy—nerve damage caused by diabetes and obesity.

   • L. Eric Huang, M.D., Ph.D., an associate professor of neurosurgery who received $1.5 million from the National Cancer Institute (NCI), will investigate a master regulator of oxygen equilibrium activated when the body doesn’t get enough oxygen to see if it plays a role in tumor development and progression.

The NIH originally funded Pulst’s research into degenerative ataxias (loss of muscle control) in 1996. Through his prior research into families with neurodegenerative diseases, Pulst discovered a gene that causes the nerve cells (neurons) to degenerate in the cerebellum. Patients with a mutation in this gene progressively lose coordination and develop features of Parkinson disease. With the latest grant, he will build on his earlier work and his recent discoveries in mutations in ion channels to search for new therapies for neurodegenerative diseases. Ions are electrically charged atoms that flow through special channels from one cell to another, determining the ability of cells to communicate.

Neuropathy is a progressive injury to the longest nerves of the body, typically affecting sensation in the toes, then progressing slowly up the leg. Along with causing pain, numbness, and weakness in the feet and, sometimes, hands, peripheral neuropathy can lead to reduced mobility, foot ulcers, and even amputation. The most common cause is diabetes, but Singleton and Smith have found that injury to these longest nerve fibers may occur with mild elevations of blood sugar, even before diabetes is present. They have shown an association between neuropathy and features of metabolic dysfunction—obesity, high blood pressure, and high cholesterol—that often occur along with high glucose as part of the Metabolic Syndrome.  The researchers suspect these related problems may damage nerves and interfere with nerve regeneration.

Singleton and Smith will use the ADA grant to compare the ability of nerves to regenerate in patients with normal metabolism, metabolic syndrome, and diabetes, and study whether intensive diet and exercise can improve nerve regeneration in each group. With the NIH grant, the two researchers will enroll patients with diabetes but no complaints of neuropathy to investigate whether an aggressive program of diet and exercise can slow or reverse injury to nerve fibers that reach to the feet and reduce progression to neuropathy.

Huang will use his $1.5 million grant from the National Cancer Institute to study how an oxygen-responsive protein factor that is activated when the body doesn’t get enough oxygen (hypoxia) may be involved in tumor growth and progression. Hypoxia has been associated with increased genetic instability in cancers, and Huang’s recent research has shown that the hypoxia-inducible factor (HIF), produced when the body responds to hypoxia, inhibits genes that help repair DNA. This suggests the obstruction of DNA repair may have a role in tumor growth and progression.

Huang also will study another, nearly identical, form of hypoxia inducible factor that does not inhibit DNA repair to examine its role in tumor growth and progression.

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