The next several years hold promise for important advances in the treatment of alcoholism, from preventing alcoholic liver disease to targeting non-neuronal central neuroimmune responses associated with chronic alcohol abuse. Further investigation is needed to determine whether indirect effects from peripheral cytokines crossing the BBB or direct effects of TLR signaling in the brain are responsible for neuroinflammation. Another limitation that needs to be addressed is an incomplete knowledge of the cellular location of cytokine receptors in the brain, which impedes our ability to tease apart glial and neuronal contributions in neuroimmune modulation of the development, progression, and persistence of alcohol addiction.
