Aggression is a behavior with evolutionary origins, but is often both destructive and maladaptive in today's society. Research over the past several decades has confirmed the involvement of neurotransmitter function in aggressive behavior. This research has centered around the "serotonin hypothesis." As this literature continues to grow, guided by pre-clinical research and aided by the application of increasingly sophisticated neuroimaging methodology, a more complex picture has emerged. As current pharmacological and therapeutic interventions are effective but imperfect, it is hoped that new insights into the neurobiology of aggression will reveal novel avenues for treatment of this destructive and costly behavior.

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Purpose of review Aggressive behavior has adaptive value in many natural environments; however, it places substantial burden and costs on human society. For this reason, there has long been interest in understanding the neurobiological basis of aggression. This interest, and the flourishing of neuroimaging research in general, has spurred the development of a large and growing scientific literature on the topic. As a result, a neural circuit model of aggressive behavior has emerged that implicates interconnected brain regions that are involved in emotional reactivity, emotion regulation, and cognitive control. Recent findings Recently, behavioral paradigms that simulate provocative interactions have been adapted to neuroimaging protocols, providing an opportunity to directly probe the involvement of neural circuits in an aggressive interaction. Here we review neuroimaging studies of simulated aggressive interactions in research volunteers. We focus on studies that use a well-validated laboratory paradigm for reactive physical aggression and examine the neural correlates of provocation, retaliation, and evaluating punishment of an opponent. Summary Overall, the studies reviewed support the involvement of neural circuits that support emotional reactivity, emotion regulation, and cognitive control in aggressive behavior. Based on a synthesis of this literature, future research directions are discussed.

Social cognitive impairment in schizophrenia is common and associated with poor functional outcome. While correlations in the moderate range suggest that social cognition and neurocognition are separate but overlapping domains, less is known about whether intact neurocognition represents a “necessary but not sufficient” condition for intact social cognition, as has been suggested. In the present study we examined the following in a sample of 119 psychiatrically stable outpatients with schizophrenia: 1) correlations between multiple social cognitive measures and neurocognition, 2) the predictive value of neurocognitive domains in explaining social cognitive performance, and 3) the co-occurrence of social cognitive and neurocognitive impairment within participants. While ¼ of participants showed intact overall neurocognition and impaired overall social cognition, only one participant had normal-range social cognition and impaired neurocognition. Results support the notion that normal range neurocognition is a necessary though not necessarily sufficient building block for good social cognitive performance.