These data may open the door for new therapeutic

Science (July 14, 2008)

damage to brain tissue as Huntington's disease may be caused by overactive immune response in blood and brain, according to new results of two teams of researchers from the University of Washington in Seattle and University College of London. Results will be published online July 14 in the Journal of Experimental Medicine. Working separately, two teams found evidence in both brain and blood cells suggests an important link between the immune system and Huntington's disease. Together, the results may help scientists find biological markers for monitoring disease progression earlier and with greater accuracy and can assist them in developing new treatments for this disease. Huntington is a fatal inherited neurodegenerative disorder for which there is currently no effective treatment. UW team led by Dr. Thomas Mueller, Research Associate Professor of Neurology, previously studied the role of inflammation and immune response in neurodegenerative diseases like Huntington's and ALS, also known as Lou Heriha disease. In this study, they found that patients with Huntington's had higher levels of immune system signaling molecules called cytokines in brain tissue. UW researchers looked at a mouse-oriented model of the disease by studying the reaction of microglia, immune cells of the nervous system. When microglia were treated starting molecule of the immune response in mice microglia Huntington produced much higher levels of cytokines, molecules of the immune system. This finding suggests that the protein produced by the Huntington's disease genetic mutation, a protein called Huntingtin, causes immune cells to be hyperactive. Researchers believe that too strong an immune response may be the mechanism by which this disease causes damage to neurons in the brain. When we found increased levels of cytokines in the brain of patients with Huntington's disease, we were very pleased, said Moller. Inflammation in the brain are increasingly recognized as an important component in other neurodegenerative diseases such as Alzheimer's or Parkinson's disease. These data may open the door for new therapeutic approaches for Huntington's disease that goal inflammation. The team from University College London focused their work on immune cells in the blood, and obtained similar results link the disease of the immune response of the body. A similar effect in patients with Huntington's that we have opened a new path in disease that mutant protein may cause damage, Moeller explained. Protein may cause damage through an abnormally overactive immune system, both in blood and brain. While damage from Huntington, usually seen in the brain, this new path is quite easy to detect in the blood of patients, so we may have found a unique window of blood that makes disease in the brain. Immune responses in the blood may also help researchers use immune system molecules of biological markers of disease that may be difficult to diagnose early. Better tracking the progression of Huntington's disease can help researchers to set up measures aimed at slowing the disease before it is reflected as brain tissue. Hentynhtona affects about 30,000 people in the United States. It is characterized by loss of motor control and cognitive function and depression or other mental disorders. And the UW and University College London research projects were supported by CHDI, Inc, a nonprofit organization that provides funds for medical research Huntington. Recommend this story on Facebook, Twitter

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