The common neuroimmune link among MDD, PTSD, and AUD suggests that neuroimmune pharmacotherapies may be particularly useful for individuals with co-occurring neuropsychiatric disorders. More research is needed to identify the genetic determinants underlying drug-induced immune activation in comorbid patients, especially in light of the polymorphisms found in P2X7Rs in treatment outcomes for mood disorders in patients with comorbid AUD (Soronen et al., 2011). In addition, AUD shares etiologies with other SUDs, often involving dysfunction of the same brain circuits and neurotransmitter systems (Koob and Volkow, 2016). Overlapping mechanisms of glial activation and neuroimmune regulation of behavior may identify shared targets for different substances of abuse. Drugs of abuse may also produce additive effects on neuroimmune activation (Alshehri et al., 2017; Althobaiti et al., 2016), and treatment efficacy may depend on the particular substances abused (Sari et al., 2016). This raises important considerations given that a majority of individuals who die from drug abuse worldwide are polydrug abusers (Preedy, 2016). Better preclinical models and more clinical investigation of comorbid psychiatric and substance use disorders will be essential to elucidate proper treatment strategies.
