Tory Hagen

Tory Hagen is a Professor in the Department of Biochemistry and Biophysics and holds the Burgess and Elizabeth Jamieson Endowed Chair in Healthspan Research in the Linus Pauling Institute, OSU. 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 understanding the fundamental events in the aging process which, if discerned, may also lead to effective therapies for a number of age-related diseases.

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Tory Hagen

My Research

The goal of my research is to discern basic cellular processes involved in elevating the risk for poor health as one ages. To accomplish this goal, we 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. We showed 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. Our lab also recently demonstrated 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). We postulate that a vicious downward spiral of mitochondrial damage and dysfunction occurs as one ages, which ultimately impacts overall cell function.

Our 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, we 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. Our data thus provides a molecular target to intervene and hopefully to lower vulnerability to environmental insults.

Finally, a key facet of our research seeks to determine whether certain dietary factors that we 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 our goal to determine whether these age-essential micronutrients also improve elder health.

Current funding

R01 AG17141A (Hagen, PI) 09/01/07 – 08/31/12
NIH/NIA
Role:  PI
Dietary Prevention of Cardiac Mitochondrial Aging

P01 AT002034 (Frei, PI) 07/01/08 – 06/30/13
NIH/NCCAM
Role:  Project Leader (Lower Vulnerability to Toxins in Aging by Treatment with Lipoic Acid)
CER on CAM Antioxidant Therapies (CERCAT)