Aging mechanisms
- *Nara Institute of Science and Technology, Department of Biological Science, 8916-5, Takayama, Ikoma, Nara 630-0101, Japan; ‡University of Texas, Southwest Medical Center, P.O. Box 9072, 5323 Harry Hines Boulevard, Dallas, TX 75235; §Tokyo Institute of Technology, Department of Life Science, 4259 Nagatsuta, Yokohama 226-8501, Japan
Abstract
Aging (senescence) has long been a difficult issue to be experimentally analyzed because of stochastic processes, which contrast with the programmed events during early development. However, we have recently started to learn the molecular mechanisms that control aging. Studies of the mutant mouse, klotho, showing premature aging, raise a possibility that mammals have an “anti-aging hormone.” A decrease of cell proliferation ability caused by the telomeres is also tightly linked to senescence. Frontier experimental studies of aging at the molecular level are leading to fascinating hypotheses that aging is the price we had to pay for the evolution of the sexual reproduction system that produces a variety of genetic information and complex body structures.
Footnotes
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↵ † To whom reprint requests should be addressed. E-mail: yotayota{at}bs.aist-nara.ac.jp.
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This paper is a summary of a session presented at the second annual Japanese–American Frontiers of Science symposium, held October 1–3, 1999, at the International Conference Center, Tsukuba, Japan.
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Article published online before print: Proc. Natl. Acad. Sci. USA, 10.1073/pnas.210382097.
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Article and publication date are at www.pnas.org/cgi/doi/10.1073/pnas.210382097
- Abbreviation:
- SPB,
- spindle pole body
- Copyright © 2000, The National Academy of Sciences
