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To: makin_dough99 who wrote (773)7/19/1998 2:16:00 AM
From: firstman  Read Replies (1) | Respond to of 4028
 
Telomerase and the aging cell: implications for human
health.

Fossel M

Department of Medicine, Michigan State University College of Human Medicine, East Lansing,
USA. Mfossel@aol.com

JAMA 1998 Jun 3;279(21):1732-1735

Recent research has shown that inserting a gene for the protein component of telomerase into
senescent human cells reextends their telomeres to lengths typical of young cells, and the cells then
display all the other identifiable characteristics of young, healthy cells. This advance not only
suggests that telomeres are the central timing mechanism for cellular aging, but also demonstrates
that such a mechanism can be reset, extending the replicative life span of such cells and resulting in
markers of gene expression typical of "younger" (ie, early passage) cells without the hallmarks of
malignant transformation. It is now possible to explore the fundamental cellular mechanisms
underlying human aging, clarifying the role played by replicative senescence. By implication, we
may soon be able to determine the extent to which the major causes of death and disability in aging
populations in developed countries-cancer, atherosclerosis, osteoarthritis, macular degeneration, and
Alzheimer dementia--are attributable to such fundamental mechanisms. If they are amenable to
prevention or treatment by alteration of cellular senescence, the clinical implications have few
historic precedents