This is an application for a cooperative agreement (U54), "Mechanisms of Alcoholic Pathology" (MAP), between faculties of the Biomedical/Biotechnology Research Institute (BBRI) at North Carolina Central University (NCCU), a Minority-Serving Institution, and the Bowles Center for Alcohol Studies at The University of North Carolina (UNC) School of Medicine. This proposal represents a true collaborative effort between the NCCU and UNC faculty with both groups contributing significant effort and being essential to the success of this CMARCD Program. Within this proposal, an NCCU Administrative component and three Research Components will integrate with the UNC-ARC Administrative, Education, 5 Research Components, and Cores, as well as other activities at the Bowles Center for Alcohol Studies. The UNC-ARC investigates mechanisms of alcohol pathology across the spectrum of behavioral, tissue, and cellular pathologies that occur with alcohol exposure. This proposal will focus on cellular pathologies that easily integrate into the ongoing overall theme of the UNC-ARC. Thus, both the UNC-ARC research components and this U54 proposal are integrated around the central theme that alcohol-induced pathology involves molecular and cellular changes that occur with alcohol abuse and alcoholism. The objectives of this U54 partnership are: 1) To investigate molecular mechanisms of alcohol-induced cellular pathology. By conducting an integrated and focused investigation into the molecular mechanisms of alcohol pathology this proposal will make important contributions to understanding alcohol morbidity and will create an active and successful research program on alcohol pathology at NCCU;2) To provide scholarly education on Alcohol Pathology. The educational efforts in this proposal will educate NCCU students on alcohol pharmacology and alcohol related pathologies and health disparities through a combined Annual Alcohol Research Day, new alcohol course curricula developed by NCCU faculty, an alcohol seminar series hosted by the BBRI, the UNC Bowles Center for Alcohol Studies seminar series, and NCCU fellowships to students on alcohol pathology and minorities. Ultimately, this proposal will conduct, promote, support, and mentor research into mechanisms of alcohol pathology, creating an acfive and successful alcohol research program within the NCCU-BBRI that synergizes with the UNC-ARC to advance education and discoveries.

Agency
National Institute of Health (NIH)
Institute
National Institute on Alcohol Abuse and Alcoholism (NIAAA)
Type
Specialized Center--Cooperative Agreements (U54)
Project #
5U54AA019767-04
Application #
8508756
Study Section
Special Emphasis Panel (ZAA1-DD (01))
Program Officer
Reilly, Matthew
Project Start
2010-08-01
Project End
2015-07-31
Budget Start
2013-08-01
Budget End
2014-07-31
Support Year
4
Fiscal Year
2013
Total Cost
$129,450
Indirect Cost
$41,984
Name
University of North Carolina Chapel Hill
Department
Pharmacology
Type
Schools of Medicine
DUNS #
608195277
City
Chapel Hill
State
NC
Country
United States
Zip Code
27599
Crews, Fulton T; Vetreno, Ryan P (2016) Mechanisms of neuroimmune gene induction in alcoholism. Psychopharmacology (Berl) 233:1543-57
Crews, Fulton T; Vetreno, Ryan P; Broadwater, Margaret A et al. (2016) Adolescent Alcohol Exposure Persistently Impacts Adult Neurobiology and Behavior. Pharmacol Rev 68:1074-1109
Vetreno, Ryan P; Yaxley, Richard; Paniagua, Beatriz et al. (2016) Adult rat cortical thickness changes across age and following adolescent intermittent ethanol treatment. Addict Biol :
Vetreno, Ryan P; Crews, Fulton T (2015) Binge ethanol exposure during adolescence leads to a persistent loss of neurogenesis in the dorsal and ventral hippocampus that is associated with impaired adult cognitive functioning. Front Neurosci 9:35
Liu, Yao; Chen, Hao; Sun, Zheng et al. (2015) Molecular mechanisms of ethanol-associated oro-esophageal squamous cell carcinoma. Cancer Lett 361:164-73
Zou, Jian Y; Crews, Fulton T (2014) Release of neuronal HMGB1 by ethanol through decreased HDAC activity activates brain neuroimmune signaling. PLoS One 9:e87915
Qin, Liya; Crews, Fulton T (2014) Focal thalamic degeneration from ethanol and thiamine deficiency is associated with neuroimmune gene induction, microglial activation, and lack of monocarboxylic acid transporters. Alcohol Clin Exp Res 38:657-71
Vetreno, Ryan P; Broadwater, Margaret; Liu, Wen et al. (2014) Adolescent, but not adult, binge ethanol exposure leads to persistent global reductions of choline acetyltransferase expressing neurons in brain. PLoS One 9:e113421
Qin, Liya; Liu, Yuxin; Hong, Jau-Shyong et al. (2013) NADPH oxidase and aging drive microglial activation, oxidative stress, and dopaminergic neurodegeneration following systemic LPS administration. Glia 61:855-68
Crews, Fulton T; Qin, Liya; Sheedy, Donna et al. (2013) High mobility group box 1/Toll-like receptor danger signaling increases brain neuroimmune activation in alcohol dependence. Biol Psychiatry 73:602-12

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