Increasing evidence suggests that the immune and neuroimmune systems play a critical role in the development and maintenance of alcohol use disorder. The immune system, which is essential for humans’ well-being, is comprised of both innate and adaptive immune mechanisms and serves as the body’s primary defense against pathogens. Preclinical animal models have provided strong support for the neuroimmune hypothesis of AUD. Clinical work has also evidenced that levels of systemic inflammation are elevated in samples of AUD.
Given the preclinical and clinical evidence, treatment targets, such as peripheral and neural immune pathways, represent an important direction in the development of novel and more effective treatment options for AUD. One promising medication is ibudilast, a neuroimmune modulator. We have completed a randomized controlled trial of ibudilast in non-treatment-seekers with an alcohol use disorder. We found that ibudilast reduced rates of heavy drinking and neural alcohol cue-reactivity compared with placebo, and found that ventral striatal alcohol cue-reactivity interacted with ibudilast to predict reductions in drinking. Ibudilast was well-tolerated in the two-week trial, as there were no significant differences between medication groups in the occurrence of adverse events.
We are currently evaluating ibudilast in a 12-week randomized clinical trial in treatment-seeking individuals with AUD (NCT03594435). The trial’s primary outcome is reduction in percent heavy drinking days with secondary outcomes targeted at examining the effects of ibudilast on peripheral markers of inflammation and depressive symptomology.
Given the preclinical and clinical evidence, treatment targets, such as peripheral and neural immune pathways, represent an important direction in the development of novel and more effective treatment options for AUD. One promising medication is ibudilast, a neuroimmune modulator. We have completed a randomized controlled trial of ibudilast in non-treatment-seekers with an alcohol use disorder. We found that ibudilast reduced rates of heavy drinking and neural alcohol cue-reactivity compared with placebo, and found that ventral striatal alcohol cue-reactivity interacted with ibudilast to predict reductions in drinking. Ibudilast was well-tolerated in the two-week trial, as there were no significant differences between medication groups in the occurrence of adverse events.
We are currently evaluating ibudilast in a 12-week randomized clinical trial in treatment-seeking individuals with AUD (NCT03594435). The trial’s primary outcome is reduction in percent heavy drinking days with secondary outcomes targeted at examining the effects of ibudilast on peripheral markers of inflammation and depressive symptomology.
