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A quick look at the supermarket newsstands reminds us we live in a culture where youth is celebrated. The magazines on display offer a variety of tonics and creams that cover the worst effects of advancing age. Between you and me, most of these treatments and procedures don't really work or merely delay the inevitable. But what does science say about the subject — are there legitimate hopes for maintaining our youth and increasing our longevity?
Actually, science already suggests we can live longer simply by severely reducing our intake of calories — referred to as caloric restriction. Studies in different animals have clearly shown reducing food intake slows down a variety of metabolic processes and can considerably extend lifespan. I don't know about you, but semi-starvation is not in the cards for me — after all, quality of life is also an issue.
With all of this in mind, a recent report by a research team at Mayo Clinic in Rochester, Minn. is of considerable interest. The cells that comprise our bodies have their own lifespans and are typically replaced by new cells after they die. However, some “old” or damaged cells linger in the tissues. It turns out these cells, referred to as senescent cells, accelerate aging in the organs in which they reside. Although the underlying reasons are unclear, senescent cells have a negative impact on the “younger” cells that surround them. This can result in age-related problems such as arthritis, cataracts and hardening arteries.
Furthermore, senescent cells secrete agents that stimulate the immune system and cause low-level inflammation. By preventing senescent cells from accumulating, the Mayo Clinic researchers showed they could prevent many of the negative aspects of aging. Mice that had been purged of senescent cells did not develop cataracts, did not exhibit muscle wasting and retained the fat layers in the skin (the thinning of these layers is the cause of wrinkling in old age). Unfortunately, eliminating these cells after aging has already occurred does not have an impact — you can't turn back time. However, this research opens up new possibilities for treating age-related diseases. It is of particular interest that despite their major impact, senescent cells are present in only low numbers, meaning their eradication will not overly impact the tissues.
What is the real significance of all this? It is probably not the case that any future drugs will realistically extend our lives since there are so many factors associated with aging. But it may be possible to improve the quality of our lives as we age. For example, it is known that advancing age is associated with a decline in the function of our immune systems, resulting in increased susceptibility to infectious disease. The white blood cells responsible for eradicating infections become sluggish with age or can trigger inappropriate and harmful responses. Bouts of influenza readily shrugged off by a young adult can be lethal to an elderly person. Drugs that prevent or delay decline in the aging immune system could afford the elderly some protection from such disease and make their immune systems more responsive to vaccines.
It is an area of research that holds considerable promise. Keystone Symposia is working to accelerate research in aging by holding a scientific conference on the biology of aging and disease in Tahoe City, Calif. this spring and another in Tokyo, Japan this fall. We hope that bringing together leading scientists in this field will promote the exchange of ideas and move the field in new and exciting directions. Hopefully there will be some progress before I get too old …
David L. “Woody” Woodland, Ph.D. is the Chief Scientific Officer of Silverthorne-based Keystone Symposia on Molecular and Cellular Biology, a nonprofit dedicated to accelerating life science discovery by convening internationally renowned research conferences in Summit County and worldwide. Woody can be reached at 970-262-1230 ext. 131 or woody@keystonesymposia.org.
Actually, science already suggests we can live longer simply by severely reducing our intake of calories — referred to as caloric restriction. Studies in different animals have clearly shown reducing food intake slows down a variety of metabolic processes and can considerably extend lifespan. I don't know about you, but semi-starvation is not in the cards for me — after all, quality of life is also an issue.
With all of this in mind, a recent report by a research team at Mayo Clinic in Rochester, Minn. is of considerable interest. The cells that comprise our bodies have their own lifespans and are typically replaced by new cells after they die. However, some “old” or damaged cells linger in the tissues. It turns out these cells, referred to as senescent cells, accelerate aging in the organs in which they reside. Although the underlying reasons are unclear, senescent cells have a negative impact on the “younger” cells that surround them. This can result in age-related problems such as arthritis, cataracts and hardening arteries.
Furthermore, senescent cells secrete agents that stimulate the immune system and cause low-level inflammation. By preventing senescent cells from accumulating, the Mayo Clinic researchers showed they could prevent many of the negative aspects of aging. Mice that had been purged of senescent cells did not develop cataracts, did not exhibit muscle wasting and retained the fat layers in the skin (the thinning of these layers is the cause of wrinkling in old age). Unfortunately, eliminating these cells after aging has already occurred does not have an impact — you can't turn back time. However, this research opens up new possibilities for treating age-related diseases. It is of particular interest that despite their major impact, senescent cells are present in only low numbers, meaning their eradication will not overly impact the tissues.
What is the real significance of all this? It is probably not the case that any future drugs will realistically extend our lives since there are so many factors associated with aging. But it may be possible to improve the quality of our lives as we age. For example, it is known that advancing age is associated with a decline in the function of our immune systems, resulting in increased susceptibility to infectious disease. The white blood cells responsible for eradicating infections become sluggish with age or can trigger inappropriate and harmful responses. Bouts of influenza readily shrugged off by a young adult can be lethal to an elderly person. Drugs that prevent or delay decline in the aging immune system could afford the elderly some protection from such disease and make their immune systems more responsive to vaccines.
It is an area of research that holds considerable promise. Keystone Symposia is working to accelerate research in aging by holding a scientific conference on the biology of aging and disease in Tahoe City, Calif. this spring and another in Tokyo, Japan this fall. We hope that bringing together leading scientists in this field will promote the exchange of ideas and move the field in new and exciting directions. Hopefully there will be some progress before I get too old …
David L. “Woody” Woodland, Ph.D. is the Chief Scientific Officer of Silverthorne-based Keystone Symposia on Molecular and Cellular Biology, a nonprofit dedicated to accelerating life science discovery by convening internationally renowned research conferences in Summit County and worldwide. Woody can be reached at 970-262-1230 ext. 131 or woody@keystonesymposia.org.
