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Abstract
Our understanding of the neuroimmune response to alcohol exposure and its role in the development and maintenance of Alcohol Use Disorder (AUD) has provided an avenue for discovering potential pharmacotherapies. We tested 28 compounds (many of which target inflammatory processes) for their ability to reduce drinking in High Drinking in the Dark mice (HDID), a unique genetic model of drinking to intoxication. Many (11 out of 14) compounds that reduced binge-like drinking in HDID mice had one thing in common; they increased anti-inflammatory signaling in the periphery. We found that apremilast, an FDA approved phosphodiesterase type 4 (PDE4) and tumor necrosis factor alpha (TNFa) inhibitor used for the treatment of psoriasis, significantly reduced binge-like drinking and blood alcohol levels in both HDID-1 and HDID-2 mice (0, 20, 40mg/kg; n=11- 13/sex/line/dose; p's < 0.05 for all).