The notion that HD is a trait that is caused by one particular gene is wrong. There is a great variation in the onset, symptoms and progression of HD. Many environmental factors and many genes are players in the rapidly unfolding HD mystery. With the HDL Triad you can addresses the environmental factors. Researcher Jonathan Lytton is studying genes that affect the progression of HD. --Jerry 12-Oct-01
American Physiological Society (APS) 12-Oct-01
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Banff, Alberta, Canada -- Many aspects of the brain's function are critically dependent upon changes in the concentration of Ca2+ inside brain cells where the molecule plays several important signaling roles. For example, both the moment-to-moment communication between nerve cells as well as the molecular alterations that underlie memory and learning are dependent upon changes in Ca2+ concentration. Understanding these precisely fine-tuned changes will help scientists discover new ways to address stroke and neuro-degenerative diseases.
Jonathan Lytton, Ph.D., Professor, Department of Biochemistry and Molecular Biology at the University of Calgary, Calgary, Alberta, Canada and his research colleagues are pioneers in understanding certain types of sodium and calcium exchangers (NCX) in the brain. Dr. Lytton will discuss his work, focusing on the expression pattern and the functional properties of the K-dependent NCX isoforms in the brain during his presentation at the 4th International Conference, Cellular and Molecular Physiology of Sodium-Calcium Exchange. The conference, which Dr. Lytton will chair, is a gathering of more than 100 international and inter-disciplinary experts and being sponsored by the American Physiological Society (APS) on October 10-14, 2001 in Banff, Alberta, Canada.
The concentration of Ca2+ in brain cells (as well as other cells) is regulated in space and time through the carefully orchestrated and coordinated action of many different protein molecules that transport Ca2+ across cellular membranes. It is only with a complete description of all Ca2+ transporting proteins, and the knowledge of how and where they work, that researchers will be able to understand cellular Ca2+ control fully. It is anticipated that such knowledge will provide novel potential therapeutic targets, and allow us to influence Ca2+ levels in predictable manners, so that treatments of disease and pathology associated with Ca2+ dys-regulation can begin.
In recent years, Dr. Lytton and his colleagues have discovered three new but unrelated genes whose products are expressed in brain at high levels. These gene products are transporters that move Ca2+ out of the cell across the outer membrane, relying upon Na+ and K+ ions to do so. Earlier research identified at least three other different types of transporters that can also move Ca2+ out of brain cells.
Using a combination of molecular biology, biochemistry and cell physiology, Lytton and his research team are currently investigating several members of the potassium-dependent sodium-calcium exchanger gene family, focusing first on understanding where the different proteins are located in the brain, where they reside in individual brain cells and the details of how each molecule works. It is hoped that this effort may lead to the identification of potential new therapeutic targets.