Tory Hagen
Tory M. Hagen is Principal Investigator and Helen P. Rumbel Professor for Healthy Aging Research at Linus Pauling Institute and Professor of the Department of Biochemistry and Biophysics at Oregon State University. He also heads the Diet, Genes, and Aging Core of the Center and has also been named Director of the Healthy Aging Program in the Linus Pauling Institute. He received his Ph.D. in Biochemistry from Emory University and performed post-doctoral research at the University of California-Berkeley before moving to Oregon State in 1998. His research is focused on free radicals, the mitochondrial theory of aging, and understanding the fundamental events in the aging process which, if discerned, may also lead to effective therapies for a number of age-related diseases.
The goal of his research is to discern basic cellular processes involved in elevating the risk for poor health as one ages. To accomplish this goal, he have two large NIH funded projects, which seek to i) define how mitochondrial decay increases risk for congestive heart failure with age, and ii) understand why the elderly are so vulnerable to a variety of stress insults. Mitochondria are the cell's "power plant," which converts raw fuels (food) into useful energy for the body. They also play major roles in calcium homeostasis and in regulating cellular apoptotic mechanisms (programmed cell death) and tissue renewal. Thus, any impairment in mitochondrial function could have dire consequences to the cell. The team in Tory's lab has shown that mitochondria in the aging heart becomes severely impaired with age, and contributes to loss of cardiac function -the leading cause of morbidity and mortality in the elderly. The lab has also recently shown that cardiac mitochondria accumulate free fatty acids and ceramide (a sphingolipid), which aberrantly induce high levels of free radicals that not only continually damage the mitochondria, but other important biomolecules (DNA). They postulate that a vicious downward spiral of mitochondrial damage and dysfunction occurs as one ages, which ultimately impacts overall cell function.
Their other research focus involves the well-known but poorly understood inability for older people to adequately respond to a variety of environmental stress insults (drug detoxification, oxidants, pollutants, etc.), which renders them vulnerable to loss of health. Recently, they made an important discovery indicating that a transcription factor, Nrf2, which may control expression of over 100 detoxification and antioxidant genes, becomes dysregulated with age. Thus, in times of stress cells no longer adequately respond to the challenge. Their data thus provides a molecular target to intervene and hopefully to lower vulnerability to environmental insults. Finally, a key facet of their research seeks to determine whether certain dietary factors that they have called "age-essential" micronutrients may improve either stress response mechanisms and/or mitochondrial function. In this regard, acetyl-L-carnitine and lipoic acid, two compounds found in muscle meats and green leafy vegetables, markedly improve mitochondrial function and improve stress response in rodent models of aging. It is now their goal to determine whether these age-essential micronutrients also improve elder health.
The goal of his research is to discern basic cellular processes involved in elevating the risk for poor health as one ages. To accomplish this goal, he have two large NIH funded projects, which seek to i) define how mitochondrial decay increases risk for congestive heart failure with age, and ii) understand why the elderly are so vulnerable to a variety of stress insults. Mitochondria are the cell's "power plant," which converts raw fuels (food) into useful energy for the body. They also play major roles in calcium homeostasis and in regulating cellular apoptotic mechanisms (programmed cell death) and tissue renewal. Thus, any impairment in mitochondrial function could have dire consequences to the cell. The team in Tory's lab has shown that mitochondria in the aging heart becomes severely impaired with age, and contributes to loss of cardiac function -the leading cause of morbidity and mortality in the elderly. The lab has also recently shown that cardiac mitochondria accumulate free fatty acids and ceramide (a sphingolipid), which aberrantly induce high levels of free radicals that not only continually damage the mitochondria, but other important biomolecules (DNA). They postulate that a vicious downward spiral of mitochondrial damage and dysfunction occurs as one ages, which ultimately impacts overall cell function.
Their other research focus involves the well-known but poorly understood inability for older people to adequately respond to a variety of environmental stress insults (drug detoxification, oxidants, pollutants, etc.), which renders them vulnerable to loss of health. Recently, they made an important discovery indicating that a transcription factor, Nrf2, which may control expression of over 100 detoxification and antioxidant genes, becomes dysregulated with age. Thus, in times of stress cells no longer adequately respond to the challenge. Their data thus provides a molecular target to intervene and hopefully to lower vulnerability to environmental insults. Finally, a key facet of their research seeks to determine whether certain dietary factors that they have called "age-essential" micronutrients may improve either stress response mechanisms and/or mitochondrial function. In this regard, acetyl-L-carnitine and lipoic acid, two compounds found in muscle meats and green leafy vegetables, markedly improve mitochondrial function and improve stress response in rodent models of aging. It is now their goal to determine whether these age-essential micronutrients also improve elder health.
Country:
USA