Key Protein May Lead to Faster Acting Anti-Depression Drugs
Posted on: Monday, 23 March 2009, 16:23 CDT
This study, Role of p11 in Cellular and Behavior Effects of 5-HT4 Receptor Stimulation, solidifies the protein p11 as a key determinant of vulnerability to depression. This new research shows that p11 activates a serotonin receptor in the brain known for producing rapid antidepressant response.
"There is pressing clinical need for faster-acting antidepressants," says Greengard. "An understanding of the cellular mechanisms underlying the therapeutic actions of these drugs may lead to better treatments with fewer side effects." In fact, each year over 17 million American adults experience at least one episode of clinical depression. Depression experts claim that many people with a depressive illness never seek treatment. Perhaps if there were antidepressants available that could start working in hours or days rather than weeks or months, more people would seek treatment.
Previous research by Greengard, who was awarded the 2000 Nobel Prize in Medicine or Physiology, helped establish p11 as an important protein that regulates signaling in the brain by the neurotransmitter serotonin, which has long been linked to mood.
The Michael Stern Parkinson's Research Foundation vision is a world without Parkinson's disease. To accomplish their vision, and cognizant that Parkinson's disease is the world's second most prevalent neurological disease after Alzheimer's, The Michael Stern Parkinson's Research Foundation mission is to fund promising, intensive, scientific and medical research that will delay Parkinson's onset, reduce the severity of its symptoms and provide better treatments, as well as fund research into related neurological diseases that can lead to a Parkinson's cure and, through education of health care professionals and the public, attempt to improve the quality of life of Parkinson's patients and their caregivers and families. www.ParkinsonInfo.org
SOURCE The Michael Stern Parkinson's Research Foundation
Source: PR Newswire
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