Research Interests
Mental disease, including addiction and neurodegeneration, are central themes of the laboratory's research. Addiction has many components, one of which is long term changes in gene expression and structure in brain. Binge drinking-induced changes in specific brain regions is hypothesized to contribute to the progression to addiction. This could overlap with brain structure/function changes in other mental diseases, particularly depression. The mechanisms of binge drinking-induced brain damage are not clearly understood but appear to involve oxidative changes in brain similar to aging and neurodegenerative disorders such as Alzheimer's disease. Alcoholics are known to have reduced brain mass which begins to grow back during recovery. Recent studies have suggested that neuroinflammation may contribute to degeneration and loss of neurogenesis during binge drinking. In contrast to the degeneration found during binge drinking there is a regeneration of brain cells during abstinence that could be related to recovery from addiction. Three key areas are investigated using rat models: the mechanisms, characteristics and functional consequences of binge drinking-induced brain damage. Histochemical, neurochemical and gene induction studies investigate the changes in brain and associated behaviors found with binge drinking induced brain damage. Current studies suggest that neuroinflammation contributes to degeneration and loss of neurogenesis, whereas regeneration during abstinence-recovery is related to increased neurogenesis.
A second area of research interest involves stem cells, which are found in specific brain regions and form new neurons. These stem cells could be involved in the regeneration of the brain during recovery from addiction. Binge drinking reduces proliferation of neural progenitor cells in brain.
A third area of research involves the use of gene delivery to understand how alterations in genes alter brain function and behavior.
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Center Line Articles
Recent Publications
Click for full publication list on PubMed
Impulsivity, frontal lobes and risk for addiction. Crews FT, Boettiger CA. Pharmacol Biochem Behav. 2009 Sep;93(3):237-47.
Deficits in adult prefrontal cortex neurons and behavior following early post-natal NMDA antagonist treatment. Coleman LG Jr, Jarskog LF, Moy SS, Crews FT. Pharmacol Biochem Behav. 2009 Sep;93(3):322-30.
Abstinence from moderate alcohol self-administration alters progenitor cell proliferation and differentiation in multiple brain regions of male and female P rats. He J, Overstreet DH, Crews FT. Alcohol Clin Exp Res. 2009 Jan;33(1):129-38.
Mechanisms of neurodegeneration and regeneration in alcoholism. Crews FT, Nixon K. Alcohol Alcohol. 2009 Mar-Apr;44(2):115-27.
Nixon K, Kim DH, Potts EN, He J, Crews FT. Distinct cell proliferation events during abstinence after alcohol dependence: microglia proliferation precedes neurogenesis.Neurobiol Dis. 2008 Aug;31(2):218-29.
Stevenson JR, Schroeder JP, Nixon K, Besheer J, Crews FT, Hodge CW. Abstinence following Alcohol Drinking Produces Depression-Like Behavior and Reduced Hippocampal Neurogenesis in Mice.Neuropsychopharmacology. 2008 Jun 18.
Liu Y, Qin L, Wilson B, Wu X, Qian L, Granholm AC, Crews FT, Hong JS. Endotoxin induces a delayed loss of TH-IR neurons in substantia nigra and motor behavioral deficits. Neurotoxicology. 2008 Sep;29(5):864-870.
Qin L, He J, Hanes RN, Pluzarev O, Hong JS, Crews FT. Increased systemic and brain cytokine production and neuroinflammation by endotoxin following ethanol treatment. J Neuroinflammation. 2008 Mar 18;5(1):10.
He J, Crews FT. Increased MCP-1 and microglia in various regions of the human alcoholic brain. Exp Neurol. 2008 Apr;210(2):349-58. Epub 2007 Dec 3.
Nicholas PC, Kim D, Crews FT, Macdonald JM. 1H NMR-based metabolomic analysis of liver, serum, and brain following ethanol administration in rats. Chem Res Toxicol. 2008 Feb;21(2):408-20. Epub 2007 Dec 21.
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Bowles Center for Alcohol Studies at the University of North Carolina at Chapel Hill