Increasing evidence suggests that chronic smoking in community-dwelling participants is associated with diminished function of multiple neurocognitive abilities and neurobiological abnormalities. The cumulative pattern of neurocognitive findings suggests dysfunction prominently in neurocircuitry implicated in decision making, impulse control, judgment, planning and reasoning skills, and in the initiation and maintenance of substance use disorders [184–187]. Specifically, the pattern of the neurocognitive and neurobiological findings in chronic smokers points to abnormalities in the brain reward system [186–188]. Major components of the brain reward system include (but are not limited to) the dorsolateral prefrontal cortex, orbitofrontal cortex, insula, anterior cingulate cortex, hippocampus, amygdala, nucleus accumbens, ventral tegmental area and other nuclei in the basal forebrain and ventral pallidum [186,189–191]. Plastic changes in the brain reward system are implicated in the development and maintenance of all substance use disorders, including nicotine dependence, and other maladaptive behaviors [186–188,192–194]. However, the actual mechanisms promoting the neurocognitive and neurobiological abnormalities reported in chronic smokers are unclear and premorbid variables(e.g., genetic vulnerabilities) must also be considered as potential contributing factor. More specifically, the neurobiological and neurocognitive abnormalities reported
