Protein Linked with Rare Disease Plays Role in Aging
CHICAGO (Reuters) - The same mechanism that causes children with a rare genetic disease called progeria to age at seven times the normal rate may play a role in normal aging as well, government researchers said on Monday.
The study led by Dr. Francis Collins, director of the National Institutes of Health, suggests aging may not simply be a gradual wearing out of cells.
Instead, it may be an active biological mechanism -- one that might be tinkered with to address age-related diseases.
"I think a lot of people in the past have assumed that the aging of cells and of individuals was just a matter of everything running down," Collins told Reuters in a telephone interview.
"What we are learning at the cellular level ... is that is not right," said Collins, whose study appears in the Journal of Clinical Investigation.
Scientists for several years have been working to understand the key biological processes that trigger aging in hopes of discovering new drugs that could delay or prevent age-related diseases such as cancer, heart disease and Alzheimer's disease.
Much of that has been focused on studying protective caps on the tips of chromosomes called telomeres, which Collins likens to "the aglets on shoelaces that keep the laces from them from getting ratty."
When telomeres become too short and frayed through cell division, the cell eventually dies. But it has not been entirely clear how this comes about.
Based on the study by Collins and colleagues at the National Human Genome Research Institute, it now appears that the same toxic protein that drives the premature aging disorder progeria plays a key role in normal cell aging, Collins said.
Formally known as known as Hutchinson-Gilford Progeria Syndrome, progeria is an extremely rare disease in which children experience symptoms normally linked with old age -- hair loss, wrinkled skin, clogged arteries and arthritis. …