B.S., N.Y. State Regents Scholar, Syracuse University , 1971
Ph.D., Pharmacology, Rackham Graduate School, University of Michigan, 1978
National Institutes of Health, Bethesda, MD , 1980
Fulton T. Crews is a neuropsychopharmacologist who for many years has investigated how drugs change the brain and behavior. He has studied antidepressants, anxiolytics, cognitive enhancers and age related neurodegeneration as well as basic neurochemical processes involved in neurodegeneration and more recently brain regeneration. As director of the UNC Bowles Center for Alcohol Studies he has investigated how chronic ethanol induces structural and functional changes in the brain associated with binge drinking to determine if and how these changes contribute to behavioral changes that lead to addiction.
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.
Representative Publications (for full publication list on PubMed, click here):
- Chronic ethanol increases systemic TLR3 agonist-induced neuroinflammation and neurodegeneration. Qin L, Crews FT.J Neuroinflammation. 2012 Jun 18;9:130.
- Inflammasome-IL-1β Signaling Mediates Ethanol Inhibition of Hippocampal Neurogenesis. Zou J, Crews FT. Front Neurosci. 2012;6:77. Epub 2012 May 30
- Postnatal day 7 ethanol treatment causes persistent reductions in adult mouse brain volume and cortical neurons with sex specific effects on neurogenesis.Coleman LG Jr, Oguz I, Lee J, Styner M, Crews FT. Alcohol. 2012 Sep;46(6):603-12.
- ATP-P2X7 receptor signaling controls basal and TNFα-stimulated glial cell proliferation. Zou J, Vetreno RP, Crews FT.Glia. 2012 Apr;60(4):661-73. doi: 10.1002/glia.22302. Epub 2012 Feb 1
- NADPH oxidase and reactive oxygen species contribute to alcohol-induced microglial activation and neurodegeneration. Qin L, Crews FT. J Neuroinflammation. 2012 Jan 12;9:5. doi: 10.1186/1742-2094-9-5.