{"id":20551,"date":"2011-02-22T09:09:27","date_gmt":"2011-02-22T14:09:27","guid":{"rendered":"https:\/\/www.ucf.edu\/news\/?p=20551"},"modified":"2019-02-28T10:04:15","modified_gmt":"2019-02-28T15:04:15","slug":"ucf-scientist-makes-breakthrough-in-huntingtons-disease","status":"publish","type":"post","link":"https:\/\/www.ucf.edu\/news\/ucf-scientist-makes-breakthrough-in-huntingtons-disease\/","title":{"rendered":"UCF Scientist Makes Breakthrough in Huntington’s Disease"},"content":{"rendered":"

A huge leap forward in understanding Huntington\u2019s disease may give patients hope for a cure.<\/p>\n

Laboratory tests on skin cells and post-mortem brain tissue of Huntington\u2019s disease patients determined that an overactive protein triggers a chain reaction that causes brain nerve cells to die. Toning down the activity of that protein, known as DRP1, prevented the chain reaction and kept those cells alive, according to the research team led by University of Central Florida Professor Ella Bossy-Wetzel.<\/p>\n

Huntington\u2019s is an inherited, incurable neurodegenerative disease affecting 35,000 people annually. The disease gradually kills nerve cells in the brain, stripping away a person\u2019s physical abilities and causing hallucinations, antisocial behavior and paranoia.<\/p>\n

People diagnosed with the disease usually die 15 to 20 years from the onset of symptoms, and there is an increased rate of suicide among those struggling with the disease.<\/p>\n

\u201cThe next step will be to test the DRP1 function in animals and patients to see whether the protein also protects the brain,\u201d Bossy-Wetzel said. \u201cThis could be done before the onset of disease in patients who have the mutant Huntington gene, but have no neurological symptoms. The hope is that we might be able to delay the onset of disease by improving the energy metabolism of the brain.\u201d<\/p>\n

The research findings were published online this week in the journal Nature Medicine<\/a>, and they will be featured in the cover story of the March edition.<\/p>\n

Until now, little has been known about how Huntington\u2019s works. Scientists knew that people with the mutant Huntington gene develop the disease. They also knew that a cell\u2019s powerhouse\u2013 mitochondria, which turn food into energy \u2013 was somehow involved. But until Bossy-Wetzel\u2019s team completed its work, little else was known.<\/p>\n

\u201cMitochondria require balanced cycles of division and fusion to maintain their ability to produce energy,\u201d Bossy-Wetzel said. \u201cThe protein DRP1 is needed for mitochondrial division. We found that in Huntington\u2019s disease, DRP1 becomes overactive and causes too much mitochondrial division without balancing fusion.\u201d<\/p>\n

That production error causes the brain\u2019s nerve cells to die. The UCF team toned down the activity of DRP1, which restored a normal balance of mitochondrial division and fusion and improved the energy metabolism and survival of neurons.<\/p>\n

Other scientists in the field say the discovery is an important step toward eventually finding a cure.<\/p>\n

\u201cIt is an outstanding piece of work, which further implicates mitochondrial dysfunction in the pathogenesis of Huntington\u2019s disease,\u201d said Flint Beal, a professor of neurology and neuroscience at the Weill Medical College of Cornell University who specializes\u00a0in the disease and is a practicing physician. \u201cIt opens new therapeutic targets for therapies aimed at disease modification.\u201d<\/p>\n

Bossy-Wetzel joined UCF’s Burnett School for Biomedical Sciences, a part of the College of Medicine, in 2007. She trained at the Cold Spring Harbor Laboratory; the University of California, San Francisco; the Pasteur Institute of Paris, France. Prior to joining UCF, Bossy-Wetzel was an assistant professor at the Burnham Institute for Medical Research in La Jolla, Calif. She has received numerous prestigious awards and her publications have received more than 8,900 citations. She serves on grant review boards for the National Institutes of Health, the National Science Foundation the Swiss National Funds, and the American Heart Association (AHA).<\/p>\n

Others who contributed to the study and appear as authors in the Nature Medicine article are UCF doctoral students Wenjun Song, Jin Chen, Alejandra Petrilli and Yue Zhou; postdoctoral fellow Geraldine Liot; and Research Professor Blaise Bossy from the UCF Burnett School of Biomedical Sciences, College of Medicine.<\/p>\n

Other collaborators include Eva Klinglmayr and Robert Schwarzenbacher, University of Salzburg, Austria; Patrick Poquiz, Jonathan Tjiong, Mark Ellisman and Guy Perkins, University of California San Diego; Eliezer Masliah, University of San Diego; Mahmoud Pouladi and Michael Hayden, University of British Columbia, Canada; and Isabelle Rouiller, McGill University, Canada.<\/p>\n","protected":false},"excerpt":{"rendered":"A huge leap forward in understanding Huntington\u2019s disease may give patients hope for a cure. Laboratory tests on skin cells and post-mortem brain tissue of Huntington\u2019s disease patients determined that an overactive protein triggers a chain reaction that causes brain nerve cells to die. 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