huntington s disease
The University of Massachusetts Medical School (UMMS) and the Lundbeck Inc., today announced a research collaboration to further develop therapies to slow or stop the progression of Huntington's disease (HD). There is currently no way to stop or reverse the course of HD, a challenging inherited neurodegenerative disease, a progressive three-motor, cognitive and emotional symptoms.1 This cooperation led to the creation of a study group of scientists to support RNAi-based therapies as a possible way to selectively suppress the production of mutant huntingtin (mHtt), the abnormal protein causes HD.2
RNA interference, or RNAi is a natural process of cell to turn off or silence the activity of specific genes. HD is assigned to a particular gene, making it a promising target for RNAi-based therapy, because the production of a mutant protein, possibly as mHtt blocked by scrapping or reducing the gene activity.3
"Our main idea is that RNAi can be used to selectively reduce the production of mutant huntingtin is slow or block the progression of HD, but it is also assumed that the excessive neural function can inhibit huntingtin gene silencing by interfering in the most important signaling events," said Aronia Neil, MD, UMMS professor of medicine and cell biology and principal investigator of the study. "This research collaboration will allow us to identify promising RNAi-based therapeutic action of selective mutant huntingtin test vehicles with the aim of restoring normal nerve function. We have a long way to push this research forward, and this is the next step Lundbeck very exciting. "
RNA interference, or RNAi is a natural process of cell to turn off or silence the activity of specific genes. HD is assigned to a particular gene, making it a promising target for RNAi-based therapy, because the production of a mutant protein, possibly as mHtt blocked by scrapping or reducing the gene activity.3
"Our main idea is that RNAi can be used to selectively reduce the production of mutant huntingtin is slow or block the progression of HD, but it is also assumed that the excessive neural function can inhibit huntingtin gene silencing by interfering in the most important signaling events," said Aronia Neil, MD, UMMS professor of medicine and cell biology and principal investigator of the study. "This research collaboration will allow us to identify promising RNAi-based therapeutic action of selective mutant huntingtin test vehicles with the aim of restoring normal nerve function. We have a long way to push this research forward, and this is the next step Lundbeck very exciting. "
