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  • These cognitive deficits may suggest that cognitive therapy

    2019-10-09

    These cognitive deficits may suggest that cognitive therapy and pharmacotherapy for gambling behavior may ultimately wish to consider genotyping as a means of better targeting treatment approaches. If core cognitive deficits are shown consistently in certain subgroups of gamblers based on genotype, then a simple saliva test may be a useful means of directing patients to more successful treatment. Because tolcapone, a COMT inhibitor, has demonstrated evidence of reversing certain cognitive deficits such as working memory in subjects with the Val/Val Vitamin D3 and (Giakoumaki et al., 2008, Farrell et al., 2012) this might be a particularly attractive medication option for gamblers with a combination of genotype and cognitive dysfunction (Grant et al., 2013). Despite this being one of the first studies to explore the clinical and neurocognitive correlates of COMT genotype in young adult gamblers, several limitations should be noted. We selected cognitive tests based on a review of the existing literature (Goudriaan et al., 2006) coupled with the need not to expose subjects to excessively long testing batteries; as such we did not quantify all relevant domains of cognition. Future work should examine other functions such as temporal discounting, Iowa Gambling Task performance, or executive planning. We did not track medication use in the subjects, and so these findings would benefit from replication in subjects who are known not to be taking medications. The issue of potential racial/ethnic differences in genotype and how this relates to gambling is clinically important, but our study was not powered or designed to address this issue, which merits attention in its own right in a future study. We could find no obvious impact of racial/ethnic group on the COMT polymorphism distribution in our sample.
    Funding
    Contributors Jon Grant: Dr. Grant designed the study, collected the data and drafted the manuscript. Eric Leppink: Mr. Leppink collected the data and assisted in drafting the manuscript. Sarah Redden: Ms. Redden collected the data and assisted in drafting the manuscript. Brian Odlaug: Mr. Odlaug assisted in drafting the manuscript. Samuel Chamberlain: Dr. Chamberlain assisted in drafting the manuscript.
    Conflicts of interest
    Acknowledgments
    Benign migratory glossitis (BMG), also known as , is a common oral mucosal lesion that usually affects the dorsal and lateral surfaces of the tongue. BMG is characterized by erythematous areas, representing papillary atrophy, surrounded by a whitish peripheral zone. These areas vary widely in appearance, size, number, and location as a result of healing of one edge and proliferation of another. They frequently disappear, recur, and coalesce in variable proportions so that the lesions appear to migrate, creating a map-like pattern that constantly changes. In most cases, BMG is asymptomatic, but patients can report sensitivity and burning sensation when acidic drinks and spicy foods are consumed. The etiology of this complex condition is not fully understood. The literature suggests that there are immunologic and psychological parameters associated with BMG and that these may be risk factors for this condition. Anxiety, the presence of a fissured tongue, and a high DMFT (decayed-missing-filled teeth) index are also associated with BMG. Alikhani et al. demonstrated that salivary cortisol concentrations and anxiety levels in individuals with BMG were significantly higher compared with those in patients without BMG. Genetic predispositions have also been raised as possible etiologic factors. For example, polymorphism in the interleukin-6 ( gene has been associated with the occurrence of BMG. Mutations in interleukin-36 receptor antagonist gene ( were also associated with BMG. Because of the association between BMG and anxiety, it is important to investigate whether genetic polymorphisms associated with anxiety could also influence the occurrence of BMG. Catechol-O-methyltransferase (COMT) catalyzes the transfer of a methyl group from S-adenosylmethionine to catecholamines, including the neurotransmitters dopamine, epinephrine, and norepinephrine. This O-methylation results in one of the major degradative pathways of the catecholamine transmitters, inactivating catecholamines, including dopamine, noradrenaline, and adrenaline. These neurotransmitters are responsible for several physiologic processes, such as mood, cognition, stress response, and pain modulation, and anxiety disorders.