68 in spite of significant progress in elucidating

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68 In spite of significant progress in elucidating the neu- robiological underpinnings of both GD and DUD, much work remains to be done. Although strides have been made in integrating GD into preexisting models of DUD, the GD literature is still lacking in a complete and thorough under- standing of the role of dopamine in the development of the disorder, which prevents its full inclusion in these broad theoretical models of addiction. 35–36 Moreover, it is clear that neurotransmitters aside from dopamine contribute signifi- cantly to the addiction process, 54 but the empirical evidence involving serotonin, norepinephrine, and glutamate in GD is sparse. 69 Neurocognition Addictive disorders are commonly associated with cognitive deficits, although there is significant variability in observed outcomes based upon the specific substance abused, as well as the intensity and chronicity of use. In individuals with alcoholism, deficits occur in the domains of executive func- tions (EFs) and visuospatial skills, while other abilities such as language and gross motor abilities are relatively spared. 70 Fortunately, these impairments resulting from chronic use can be at least partially ameliorated with prolonged absti- nence. Individuals with GD also exhibit deficits in EFs, 71 including decision making, 72 inhibitory control, 73 and mental flexibility; 74 however, no studies to date have examined the impact of prolonged abstinence from gambling on these defi- cits. Another unresolved question in this literature pertains to whether these neurocognitive deficits are present pre- morbidly or whether they represent downstream phenotypic effects of physiological changes due to addictive behaviors. Several studies in GD and alcohol dependence generally support the presence of premorbid impulsivity in the larger population of individuals with addictions, although data from these investigations also indicate greater impairment in EFs such as working memory among individuals with alcohol dependence compared to those with GD, 75 possibly suggesting that chronic ethanol ingestion selectively damages PFC circuitry. Moreover, convergent with neurocognitive findings, self-report data show that trait impulsivity tends to be elevated in GD, providing independent, multimodal evidence for preexisting inhibitory control deficits in addic- tive disorders. 73,76 Overall, findings regarding neurocognitive deficits in GD are informative, especially with respect to investigations in which GD is utilized as a behavioral model of addiction in order to address specific research questions. 75 However, a key limitation that has persisted in this literature is heterogene- ity in cognitive tasks employed across studies, which limit direct comparisons and aggregate analyses.
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