Christiaan Leeuwenburgh, Ph.D.
Professor
Aging and Geriatrics

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Frailty and Sarcopenia, Apoptosis, and Oxidative Stress
Frailty and Sarcopenia. Frailty is a serious condition in the elderly and is characterized by impaired endurance and balance, vulnerability to injury, high risk of morbidity, disability, mortality and strength. Age-related muscle atrophy, termed sarcopenia, can have a significant effect on individual health and quality of life and is strongly associated with frailty and mortality. We are examining the extent of apoptosis in human skeletal muscle and during the progression of sarcopenia and the signal transduction pathways responsible for apoptosis in human skeletal muscle of frail, intermediate-frail and non-frail age-matched controls. Moreover, we are investigating apoptosis and mitochondrial and TNF-alpha mediated pathways responsible for apoptosis in human skeletal muscle of frail and age-matched controls.

Apoptosis. Apoptosis is a highly regulated form of cell death characterized by specific morphological, biochemical, and molecular events. However, its role during aging, particularly in post mitotic tissues such as the brain, heart and skeletal muscle has not been studied in depth. We have found that apoptosis appear to increase in post-mitotic tissues with age and it may be a major contributing factor to the observed loss in tissue function with age. The mechanisms by which apoptosis are induced with advancing age and adaptations through specific signaling transduction pathways that may protect against apoptosis remain to be identified and are under investigation.

Oxidative Stress. Oxidative damage, particularly to proteins, is widely believed to be a major cause of the loss of muscle function during senescence. We have observed decreases in mitochondrial oxidative capacity and enzyme activity with age in muscle, which may be directly related to free radical oxidant damage within the mitochondria. The mechanism responsible for this decline is unknown and may be related to increases in oxidant production and a decrease in mitochondrial bioenergetics that occurs with aging in mitochondria. Moreover, the sources of reactive radical species that contribute to protein oxidative damage are poorly understood, primarily because of the non-specific methods used to study protein, DNA and RNA oxidation. Hence, understanding the molecular mechanisms of oxidative damage and the decline in energy production in skeletal muscle with age is important for targeted interventions. 		Status:
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Contact Information:
office: Med. Sciences Bldg, P2-33
lab: Med. Sciences Bldg, P1-08, P1-09
phone: (352) 273-6796
email: cleeuwen@aging.ufl.edu
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Biography:
Christiaan Leeuwenburgh received his PhD from the University of Illinois, Urbana-Champagne in 1995 where his doctoral work focused on the regulation of glutathione homeostasis during chronic glutathione deficiencies and/or supplementation. He completed postdoctoral studies in Internal Medicine, Division of Geriatrics and Gerontology and Division of Atherosclerosis, Nutrition and Lipid Research at Washington University School of Medicine, Saint Louis.

He became an Assistant Professor in 1998 at the University of Florida and the Director of the Biochemistry of Aging Laboratory. He is currently a Professor with the Department of Aging and Geriatric Research, College of Medicine and Institute on Aging at the University of Florida and is the Chief of the Division of Biology of Aging.

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