Event Summary: Nicotine addiction is a chronic relapsing disorder driven by molecular changes that occur in the brain in response to habitual drug use, and currently available pharmacotherapies have shown only limited efficacy reducing nicotine use and relapse in addicts. Nicotine exposure produces profound changes in lipid and neuropeptide signaling during dependence and withdrawal that ultimately underlie many aspects of the resulting behavioral dysfunction, and collectively these molecules comprise a largely untapped resource of potentially druggable targets that can be directly translated into clinical therapeutics.
Our research objective is to identify and validate novel molecular signals that are dysregulated by drug exposure and other neurological disorders. To address this issue, we employed a multidisciplinary approach to identify and validate novel signaling pathways in the brain, and identified the lipids 2-arachidonoylglycerol (2-AG) and oleoylethanolamine (OEA) as two potential druggable targets of nicotine dependence. Future research will implement broad-scale lipidomic and proteomic technologies to identify new lipid and neuropeptide signaling molecules driving neulogical disorders, and develop novel therapeutics to facilitate patient treatment.Event Contact: