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Experimentally defining the genetics that shape the brain—and ultimately the behaviors it controls, such as those leading to the complex outcomes of addiction and age-related pathologies —is a challenging but promising endeavor. In this context, we use a mouse genetic approach to explore the interactions between nicotine addiction, inflammation and age-related degenerative disorders. Like humans, mice of different genetic background also exhibit remarkably different physiological mechanism(s) leading to nicotine dependence, regulation of inflammatory processes, and susceptibility to a variety of maladies experienced with age. Because we believe these processes are interactive, the mouse model appears to hold promise as a powerful tool for understanding how genetics and behavioral measures combine to individualize the physiological responses to nicotine as we age. 1/2008 |
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