PTSD is characterized by deficits in "top-down" cognitive control abilities, as evidenced by neuropsychological findings of poor executive functioning and neurobiological evidence of diminished prefrontal cortical activity coupled with exaggerated limbic activity. Cognitive control deficits are causally implicated in re-experiencing symptoms, suggesting that cognitive control may be a novel and effective treatment target. The investigator developed a cognitive control training intervention that has demonstrated initial evidence of efficacy in civilian women with PTSD secondary to sexual assault. However, the effects of this program in Veteran participants and the precise neurocognitive mechanisms of symptom reduction in the intervention remain poorly understood. If training cognitive control directly enhances functioning of specific cognitive systems that are causally implicated in the etiology of emotional and cognitive symptoms, treatment-related improvements in affective symptoms and neuropsychological performance within the trained domain would be predicted. From a neurobiological perspective, training cognition is thought to operate via modification of specific neural substrates, suggesting that training effects should generalize to affective processes relying on shared neural regions. One such affective process is reappraisal (i.e., generating different ways of thinking about emotional content in order to regulate emotion), which requires cognitive control over affective emotional information, and depends on brain circuits identified as key cognitive control regions (e.g., dorsolateral prefrontal cortex, dlPFC). PTSD is characterized by aberrant affective and neurobiological patterns during reappraisal that likely contribute to persistent re-experiencing and hyperarousal symptoms. Training may reduce symptoms by improving neural functioning of cognitive control regions during affective control processes (e.g., reappraisal) that are critical to managing trauma-related affect.