Anxiety and depressive disorders are associated with significant social and occupational impairments and lead to considerable emotional, economic, and societal burden. Trait negative affect (NA) is a crucial factor associated with increased likelihood of developing anxiety and depression, as well as vulnerability to comorbidity and relapse. However, little is known about how trait NA fosters anxiety and depression. The present dissertation aimed to clarify possible psychological and biological mechanisms through which trait NA leads to the development and maintenance of anxiety and depressive disorders in order to develop interventions that more effectively prevent their onset and recurrence. A series of studies tested the overarching hypothesis that one possible route is through triggering maladaptive cognitive and motivational processing. Trait NA appears to foster risk through dysfunction in brain regions that implement top-down attentional control in the presence of distracting information that is both emotional and nonemotional in nature. It is also associated with problems integrating motivational processes with emotional and cognitive processes. Trait NA does not appear to alter behavior, rather individuals high in trait NA are able to recruit compensatory strategies, particularly in rewarding contexts. In addition, trait NA interacts with deficits in executive function, specifically updating and shifting, to predict depressive symptoms. Present results may lead to the identification of early markers of risk for anxiety and depression that are not necessarily observable via behavior or self-report. This may foster the development of prevention strategies aimed at addressing dysfunctional processing in those individuals identified as being at risk.
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Elucidating psychological and neural mechanisms associated with risk for anxiety and depression