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Introduction
There is a large number of individuals suffering from an alcohol-use disorder (AUD) throughout the world (Bouchery, Harwood, Sacks, Simon, & Brewer, 2011; Grant et al., 2004; Harwood, 2000 ). This disorder is the third leading risk factor for premature death and disabilities and is responsible for 4% of all deaths (World Health Organization, 2011 ). In the United States, the costs associated with individuals suffering from an AUD account for nearly half of the total cost of untreated addiction, totaling over $185 billion annually (Research Society on Alcoholism, 2011 ). A significant portion of this cost is due to reduced, lost, and foregone earnings. The remainder of the cost comes from medical and treatment expenses, decline in workforce productivity, accidents, violence, and premature death. Despite the known harm caused by ethanol, current pharmacological treatment strategies are limited and have yielded only modest positive results, as indicated by the continued high prevalence of AUD. Although treatments for AUD have improved somewhat over the past two decades (Miller, Book, & Stewart, 2011 ), the continued high rate of AUD illustrates the need to develop new, more effective interventions.
Pharmacotherapies for AUD are used less often than psychosocial interventions (Fuller & Hiller-Sturmhöfel, 1999 ). However, without a pharmacological adjunct to psychosocial therapy, nearly three-quarters of patients resume drinking within 1 year (Johnson, 2008 ). The limited use of pharmacotherapy for AUD is due, in part, to the relative lack of options to successfully treat these disorders (Edlund, Booth, & Han, 2012 ). To address this issue, our research group is investigating the utility of ivermectin (IVM) as a novel pharmacotherapy for the treatment and/or prevention of AUD (Asatryan et al., 2014; Wyatt et al., 2014; Yardley et al., 2012, 2014 ).
IVM is a broad-spectrum antiparasitic avermectin (Geary, 2005; Molinari, Soloneski, & Larramendy, 2010; Richard-Lenoble, Chandenier, & Gaxotte, 2003 ). The current therapeutic potential of IVM is attributed to action on a non-mammalian, glutamate-gated inhibitory chloride channel (Cully et al., 1994; Dent, Davis, & Avery, 1997; Vassilatis et al., 1997 ). Studies in humans and rodents suggest additional sites of action for IVM not related to these receptors (Sung, Huang, Fan, Lin, & Lin, 2009