La Jolla CA., March 31, 2000 -- Gradual genetic changes may be the source of many, if not all illnesses of aging, including breast cancer, osteoporosis, Alzheimer's disease and arthritis. A new study by scientists in The Skaggs Institute for Chemical Biology at The Scripps Research Institute (TSRI) in La Jolla and the Genomics Institute of the Novartis Research Foundation, published in the latest issue of Science, concludes that human aging and its associated diseases and conditions can be traced to a gradual increase in cell division errors in tissues throughout the body. This functional change begins slowly in middle age and increases gradually with advancing age.
According to Richard A. Lerner, M.D., an author of the paper, "Mitotic Misregulation and Human Aging," "This represents a radical change in the way people have thought about aging. While scientists have believed that aging is a disease in which cells stop dividing, this study suggests that aging is really a disease of quality control. In this case the manufactured product is a new cell. As we get older, altered gene expression results in cells with diminished function." Dr. Lerner is TSRI President, Lita Annenberg Hazen Professor of Immunochemistry, Cecil H. and Ida M. Green Chair in Chemistry, and Professor in The Skaggs Institute for Chemical Biology and the Department of Chemistry. Cell Division Errors are Key
Errors in cell division lead to the altered expression of a collection of key genes in the cells. Altered gene expression gradually causes the loss of tissue function which results in aging. Unlike cancers, in which cells are uniformly dysfunctional, aging occurs in a mosaic pattern, at different rates in different parts of the body. "Our research ties the effects of aging into a single package by identifying a common element in aging tissues throughout the body," Dr. Lerner continued.
Dr. Lerner noted that, "The Human Genome Project is biology's particle physics experiment. Beca
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Contact: Robin B. Goldsmith
rgoldsmi@scripps.edu
858-784-8134
Scripps Research Institute
29-Mar-2000