Mentalizing involves the ability to predict someone else's behavior based on their belief state. More advanced mentalizing skills involve integrating knowledge about beliefs with knowledge about the emotional impact of those beliefs. Recent research indicates that advanced mentalizing skills may be related to the capacity to empathize with others. However, it is not clear what aspect of mentalizing is most related to empathy. In this study, we used a novel, advanced mentalizing task to identify neural mechanisms involved in predicting a future emotional response based on a belief state. Subjects viewed social scenes in which one character had a False Belief and one character had a True Belief. In the primary condition, subjects were asked to predict what emotion the False Belief Character would feel if they had a full understanding about the situation. We found that neural regions related to both mentalizing and emotion were involved when predicting a future emotional response, including the superior temporal sulcus, medial prefrontal cortex, temporal poles, somatosensory related cortices (SRC), inferior frontal gyrus and thalamus. In addition, greater neural activity in primarily emotion-related regions, including right SRC and bilateral thalamus, when predicting emotional response was significantly correlated with more self-reported empathy. The findings suggest that predicting emotional response involves generating and using internal affective representations and that greater use of these affective representations when trying to understand the emotional experience of others is related to more empathy.

Empathy is an important component of human relationships, yet the neural mechanisms that facilitate empathy are unclear. The broad construct of empathy incorporates both cognitive and affective components. Cognitive empathy includes mentalizing skills such as perspective-taking. Affective empathy consists of the affect produced in response to someone else's emotional state, a process which is facilitated by simulation or ‘mirroring’. Prior evidence shows that mentalizing tasks engage a neural network which includes the temporoparietal junction, superior temporal sulcus, and medial prefrontal cortex. On the other hand, simulation tasks engage the fronto-parietal mirror neuron system (MNS) which includes the inferior frontal gyrus (IFG) and the somotosensory related cortex (SRC). Here, we tested whether neural activity in these two neural networks was related to self reports of cognitive and affective empathy in daily life. Participants viewed social scenes in which the shift of direction of attention of a character did or did not change the character's mental and emotional state. As expected, the task robustly activated both mentalizing and MNS networks. We found that when detecting the character's change in mental and emotional state, neural activity in both networks is strongly related to cognitive empathy. Specifically, neural activity in the IFG, SRC, and STS were related to cognitive empathy. Activity in the precentral gyrus was related to affective empathy. The findings suggest that both simulation and mentalizing networks contribute to multiple components of empathy.

Fear and reward learning can occur through direct experience or observation. Both channels can enhance survival or create maladaptive behavior. We used fMRI to isolate neural mechanisms of observational fear and reward learning and investigate whether neural response varied according to individual differences in neuroticism and extraversion. Participants learned object-emotion associations by observing a woman respond with fearful (or neutral) and happy (or neutral) facial expressions to novel objects. The amygdala-hippocampal complex was active when learning the object-fear association, and the hippocampus was active when learning the object-happy association. After learning, objects were presented alone; amygdala activity was greater for the fear (vs. neutral) and happy (vs. neutral) associated object. Importantly, greater amygdalahippocampal activity during fear (vs. neutral) learning predicted better recognition of learned objects on a subsequent memory test. Furthermore, personality modulated neural mechanisms of learning. Neuroticism positively correlated with neural activity in the amygdala and hippocampus during fear (vs. neutral) learning. Low extraversion/high introversion was related to faster behavioral predictions of the fearful and neutral expressions during fear learning. In addition, low extraversion/high introversion was related to greater amygdala activity during happy (vs. neutral) learning, happy (vs. neutral) object recognition, and faster reaction times for predicting happy and neutral expressions during reward learning. These findings suggest that neuroticism is associated with an increased sensitivity in the neural mechanism for fear learning which leads to enhanced encoding of fear associations, and that low extraversion/high introversion is related to enhanced conditionability for both fear and reward learning.

Different individuals have different (and different-looking) significant others, friends, and foes. The objective of this study was to investigate whether these social face environments can shape individual face preferences. First, participants learned to associate faces with positive, neutral, or negative behaviors. Then, they evaluated morphs combining novel faces with the learned faces. The morphs (65% and 80% novel faces) were within the categorical boundary of the novel faces: They were perceived as those faces in a preliminary study. Moreover, a second preliminary study showed that following the learning, the morphs' categorization as similar to the learned faces was indistinguishable from the categorization of actual novel faces. Nevertheless, in the main experiment, participants evaluated morphs of "positive" faces more positively than morphs of "negative" faces. This learning generalization effect increased as a function of the similarity of the novel faces to the learned faces. The findings suggest that general learning mechanisms based on similarity can account for idiosyncratic face preferences.

Cognitive remediation training has been shown to improve both cognitive and social-cognitive deficits in people with schizophrenia, but the mechanisms that support this behavioral improvement are largely unknown. One hypothesis is that intensive behavioral training in cognition and/or social-cognition restores the underlying neural mechanisms that support targeted skills. However, there is little research on the neural effects of cognitive remediation training. This study investigated whether a 50 hour (10-week) remediation intervention which included both cognitive and social-cognitive training would influence neural function in regions that support social-cognition. Twenty-two stable, outpatient schizophrenia participants were randomized to a treatment condition consisting of auditory-based cognitive training (AT) [Brain Fitness Program/auditory module ~60 minutes/day] plus social-cognition training (SCT) which was focused on emotion recognition [~5–15 minutes per day] or a placebo condition of non-specific computer games (CG) for an equal amount of time. Pre and post intervention assessments included an fMRI task of positive and negative facial emotion recognition, and standard behavioral assessments of cognition, emotion processing, and functional outcome. There were no significant intervention-related improvements in general cognition or functional outcome. FMRI results showed the predicted group-by-time interaction. Specifically, in comparison to CG, AT+SCT participants had a greater pre-to-post intervention increase in postcentral gyrus activity during emotion recognition of both positive and negative emotions. Furthermore, among all participants, the increase in postcentral gyrus activity predicted behavioral improvement on a standardized test of emotion processing (MSCEIT: Perceiving Emotions). Results indicate that combined cognition and social-cognition training impacts neural mechanisms that support social-cognition skills.

Fragile X syndrome (FXS) is the most common inherited form of mental retardation, occurring in roughly 1/4000 males and 1/8000 females. An abnormal expansion of a trinucleotide CGG repeat sequence in the fmr1 gene results in transcriptional silencing of this gene, which codes for the Fragile X Mental Retardation Protein (FMRP). The loss of FMRP, directly and/or indirectly, gives rise to the FXS phenotype, which includes a characteristic set of anatomic and cognitive/behavioral features. The present studies were designed to test the hallmark areas of dysfunction (i.e. attention, inhibitory control, hyperarousal, and emotional regulation) seen in human FXS and further characterize spared and impaired functions in fmr1 KO mice. The performance of F1 hybrid fmr1 KO mice (a C57BL/6J x FVB/NJ cross) and wild-type (WT) littermate controls were evaluated on a series of tasks designed to assess inhibitory control and various aspects of attention, Reversal Learning Task, and Associate Learning Task. Regulation of arousal and emotion, two domains affected in FXS, was also evaluated in these tasks by examining the animals' reaction to the unexpected presentation of potent olfactory distractors (in the Distraction task), as well as their reaction to committing an error on the previous trial.The present studies provided the first evidence that the hallmark deficits in human FXS --impaired attention, inhibitory control, and arousal regulation -are also impaired in the fmr1 mouse model of FXS. In addition, these findings demonstrate that attentional dysfunction and impaired inhibitory control are most prominent when task contingencies change and when the animal has just committed an errorsituations that arouse or disturb the mice. Analysis of videotapes further demonstrates that arousal regulation is impaired in the fmr1 KO mice. Additionally, the fmr1 KO mice were not impaired in associative learning, transfer of learning, or reversal Jisook's stidies in New Generation stimulated her desire for a deeper and moe systematic understanding of the neural mechanisms of human brain. She was accepted into the Department of Psychology at Yonsei University, which is considered one of the best programs in Korea. This allowed her the unique combination of being able to study at Yonsei University and to work part time for New Generation C&C. Working and studying at the same time allowed her many opportunities to apply academic knowledge to real-world situations.To the end, Jisook assisted Dr. Kang in her lab, the Cognitive Neuroscience and Medical Physics Lab at the Seoul National University Hospital. There, she conducted studies on memory and learning in normal human conditions, as well as abnormal states of perception such as epilepsy and dementia. Through cutting-edge imaging methods (i.e. fMRI, PET, and MRI) coupled with some behavioral tests, she furthered her knowledge of functional and structural workings of the human brain iv during learning, memorizing, and recognizing. She also ganed insight into how the activity of the brain dif...

Both cognitive and social-cognitive deficits impact functional outcome in schizophrenia. Cognitive remediation studies indicate that targeted cognitive and/or social-cognitive training improves behavioral performance on trained skills. However, the neural effects of training in schizophrenia and their relation to behavioral gains are largely unknown. This study tested whether a 50-h intervention which included both cognitive and social-cognitive training would influence neural mechanisms that support social ccognition. Schizophrenia participants completed a computer-based intervention of either auditory-based cognitive training (AT) plus social-cognition training (SCT) (N=11) or non-specific computer games (CG) (N=11). Assessments included a functional magnetic resonance imaging (fMRI) task of facial emotion recognition, and behavioral measures of cognition, social cognition, and functional outcome. The fMRI results showed the predicted group-by-time interaction. Results were strongest for emotion recognition of happy, surprise and fear: relative to CG participants, AT+SCT participants showed a neural activity increase in bilateral amygdala, right putamen and right medial prefrontal cortex. Across all participants, pre-to-post intervention neural activity increase in these regions predicted behavioral improvement on an independent emotion perception measure (MSCEIT: Perceiving Emotions). Among AT+SCT participants alone, neural activity increase in right amygdala predicted behavioral improvement in emotion perception. The findings indicate that combined cognition and social-cognition training improves neural systems that support social-cognition skills.

Introduction-Failure to self-regulate after an interpersonal conflict can result in persistent negative mood and maladaptive behaviors. Research indicates that lateral prefrontal cortex (LPFC) activity is related to the regulation of emotional experience in response to lab-based affective challenges, such as viewing emotional pictures. This suggests that compromised LPFC function may be a risk-factor for mood and behavior problems after an interpersonal stressor. However, it remains unclear whether LPFC activity to a lab-based affective challenge predicts self-regulation in real-life.