By Carolyn Y. Johnson, Globe Staff
Aging may be a case of neglect -- an absentee landlord at the cellular level that allows gene activity to go awry, according to a study published today.
Scientists have long known that aging causes gene expression to change, and DNA damage to accumulate. But now, research led by Harvard Medical School scientists explains the connection between the two processes in mammals.
The paper, published in the journal Cell, found that a multi-tasking protein called SIRT1 that normally acts as guardian of the genome gets dragged away to DNA fix-it jobs. When the protein abandons its normal post to work as a genetic handyman, order unravels elsewhere in the cell. Genes that are normally under its careful watch begin to flip on.
"What this paper actually implies is that aspects of aging may be reversible," said David Sinclair, a Harvard Medical School biologist who led the research. "It sounds crazy, but in principle it should be possible to restore the youthful set of genes, the patterns that are on and off."
The study is just the latest to draw yet more attention to sirtuins, proteins involved in the aging process that have been a target for a biotech company Sinclair co-founded, Sirtris Pharmaceuticals.
What's not yet clear is how much youthful patterns of gene expression matter. Scientists not involved in the study pointed out that even if that particular aspect of aging is reversible, it is not clear that keeping gene expression young is the key to staying young.
"The paper says you might be able to maintain or go back to a younger gene expression profile, but does that mean you will be younger? You may have passed through that gate already, and you can't go back," said Dr. Stephen Helfand, a professor in the department of molecular biology, cell biology and biochemistry at Brown University.
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