Scientists have discovered that as cells age, the gene, called p16INK4a, becomes more active and certain cells in the body stop multiplying and begin deteriorating. The cells have greater protection against cancer but lose the ability to divide and cannot be replaced.

    The studies, presented in the Sept. 7 issue of the journal Nature, suggest the physical and mental breakdown that accompany aging are the result of a cellular decline that is programmed into our genes. The program is designed to safeguard us against copying mistakes that become more frequent as we grow older.

    "This research tells us why our old tissues have less regenerative capacity than young tissues," said Sean Morrison of the University of Michigan, who was involved in one of the studies. "It's not that old tissues wear out -- they're actively shutting themselves down, probably to avoid turning into cancer cells."

    Research teams from three medical schools examined the role of p16INK4a in cells taken from different parts of the body in mice.

    A team from the University of North Carolina (UNC) at Chapel Hill looked at the gene's role in pancreatic islet cells, which produce and secrete the hormone insulin and which are defective in persons with Type 1 diabetes. Another team from the University of Michigan examined brain stem cells. A third team from Harvard University looked at p16INK4a in blood stem cells.

    All three studies found that as animals got older, p16INK4a activity increased and the cells eventually stopped dividing. Cells in mice deficient in the gene continued to divide but were more likely to turn cancerous. Cells in animals with over-expression of the gene stopped dividing earlier and aged prematurely.

    The experiments also showed that cells taken from old animals remember their "age" and continue to deteriorate at their previous rate even when transplanted into young animals. Enditem

    (Agencies)