Body ageing: scientists look for more clues

Press, 28 July 1986, Page 36

Body ageing: scientists look for more clues

MALCOLM RITTER

By

or associated tress

(through NZPA)

New York

Scientists seeking clues to what makes the body age are delving into its tiniest portions, focusing on genes and a rubbishdisposal system to clean cells.

But findings are still sketchy in what scientists call a relatively new phase of ageing research. “We’re only now beginning to explore the fundamental biology of ageing,” said a researcher, Mr Leonard Hayflick, of the University of Florida. “We’re in a position now of gathering data and formulating ideas.” Mr Hayflick was one of the researchers who discussed theories of ageing recently at a symposium in New York on modern biological theories of ageing.

Some work focuses on genes, the chemical blueprints within cells. Genes guide the development of an animal from a fertilised egg to adulthood, turning on and off at different times to carry out the genetic programme for development. Some scientists wonder if

the genes later guide the body through ageing as well.

Mr Richard Russell, of the University of Pittsburgh, said studies of a tiny worm had found sizeable changes in enzyme levels after its reproductive period was largely over, suggesting that a gene might be turned on during ageing. Several human diseases that accelerated some processes seen in normal ageing showed some genetic involvement.

But the case for a genetic programme that controlled ageing was not proved yet, he said. Mr Hayflick, for his part, doubted such a programme existed. People were genetically programmed to grow old enough to reproduce, he asserted, and what happened after that was of absolutely no importance to the species. Humans had spent perhaps 99.9 per cent of their time on Earth with a life expectancy of 18 years, he said, and ageing, which came along with medical advances, could be considered simply an aberration of civilisation. Some researchers take

another tack on the influence of genes, asking if ageing involves loss of ability to repair the body’s D.N.A. — the threadlike molecules along which genes lie. Studies had suggested, for example, that there was an age-related decrease in the ability of human skin cells to fix D.N.A., said Mr Richard Setlow, of Brookhaven National Laboratory, New York. Studies also found that animal species that had tended to live longer had more active repair mechanisms, he said. On the other hand, studies of humans with diseases that included elements of premature ageing had not found consistent defects in D.N.A. repair mechanisms, he said. Another possibility for ageing research lay in a rubbish-disposal system of body cells, suggested Mr Fred Dice, associate physiology professor at the Tufts University School of Medicine, Boston. Studies of human skin cells grown in the laboratory had found agerelated declines in activity of tiny features called lysosomes. These struc-

tures helped in the cells’ routine maintenance of destroying and replacing key substances.

“It’s not known whether the decline is a cause or effect of ageing,” Mr Dice said.

Other-scientists warned that results from labora-tory-grown cells might not reflect what happened in the body.

But Mr Dice suggested when lysosomes became less active, the cell accumulated abnormal proteins, which might trigger heightened activity by a second cellular system that attacked abnormal proteins.

“But that system also destroys normal proteins the cell doesn’t need any more and when it becomes overactive, it may begin destroying needed proteins, harming key operations of the cell,” Mr Dice said.

“The most exciting thing about this (theory) is it’s specific enough that in two years we’ll know if it’s right,” he said. By then, scientists should be able to fix defective lysosomes and see if it makes any difference.