Wednesday, October 14, 2009

University Scholar Seminar - Russ Tracy

UNIVERSITY SCHOLAR SEMINAR

Presented by

Russell P. Tracy, PhD
Professor of Pathology and Biochemistry
Director, Laboratory for Clinical Biochemistry Research

Inflammation, Atherosclerosis and Aging: the Inflammation Hypothesis of Aging

 “…inflammation of the inner arterial coat [is] the starting point of the so-called atheromatous degeneration.” R. Virchow, 1859.
“Longevity is a vascular question, which has been well expressed in the axiom ‘a man is as old as his arteries.’ To a majority of men, death comes primarily or secondarily through this portal.” William Osler, 1892.
“Yep, son, we have met the enemy and he is us!” Pogo to Porky (as written by Walt Kelly), 1971

Over the last 15 years we have come to understand that the human inflammatory response is a major part of atherosclerosis, the pathophysiological process that leads to most of the heart disease in the world. This position was held by some in the past, but not well understood by most researchers and practitioners in the field until recently. Additionally, we have come to understand that inflammation as a response to a variety of stressors is part of not only atherosclerosis, but many (all?) of the chronic diseases associated with aging, such as  insulin resistance, osteoporosis, dementia and others. Our laboratory has contributed to this work through molecular, cellular, and genetic epidemiology in a variety of fields.

Because of this work, some of which we will discuss in this talk, we and others recently have proposed a broad concept, an “inflammation hypothesis of aging”. This hypothesis suggests that the cumulative lifetime burden of our own inflammatory responses, while critically important to short-term survival, plays a major role in the aging process itself.  Within this conceptual framework, we propose that the time-dependent inflammation-driven deterioration of individual organ function has multi-organ system-wide consequences, which ultimately yield an exponential decline in health (i.e., frailty and death). This decline starts at an age which appears to be at least in part driven by evolutionary biology and natural selection. We also propose that the rate of decline in any individual is a function of the environmental stresses to which she/he must respond, and the degree of response which is in turn driven by genetic architecture and physiological response capacity. Finally, we propose that within this framework, many diseases can be viewed as organ-specific accelerated aging with systemic ramifications. If validated, this view has implications for a broad range of translational research issues from pharmaceutical development to diagnostic biomarkers and the interpretation of high resolution biomedical imaging.



4:00 PM, Thursday, October 22, 2009
Memorial Lounge, Waterman Building

The University Scholar Awards Program annually recognizes distinguished faculty members for sustained excellence in research and scholarly activities.  The Scholars are selected by a panel of distinguished faculty, based upon nominations submitted by UVM colleagues.


Refreshments at 3:45 and after the Seminar
Sponsored by the Graduate College

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