Social cognition refers to how people think about themselves and others in the social world, which is considered to be the mental operations that underlie social interactions. Previous studies have shown that patients with schizophrenia exhibit extensive social cognitive impairments. These social cognitive impairments have detrimental impact upon their social function and prognosis. However, the current pharmacological and psychological interventions have limited effect to improve these impairments. According to the "glutamate hypothesis", social cognitive impairments of patients with schizophrenia may be due to the altered glutamatergic function in the brain. Studies using "magnetic resonance spectroscopy (MRS)" have provided ample evidence of the correlation of glutamate level with neurocognitive functions in patients with schizophrenia. However, few studies have been conducted to examine the correlation between glutamate level and social cognition in this clinical group.
On the other hand, individuals with schizotypy have been considered to be the subclinical group across the spectrum of schizophrenia. These individuals have been found to exhibit similar but a milder extent of social cognitive impairments comparing to schizophrenia patients. Study of individuals with schizotypy thus provides us a unique opportunity to get rid of the confounding effect of antipsychotic medication upon the observed social cognitive functions in patients with schizophrenia. It also helps us to examine and test whether the glutamate hypothesis has been presence in these at-risk individuals for schizophrenia. This dissertation comprised two studies examining the correlation between glutamate level and social cognition in patients with schizophrenia and individuals with schizotypy.
Study 1 examined the glutamate level in anterior cingulate cortex and its correlation with social cognition in 40 patients with schizophrenia and 37 healthy controls. Twenty-two patients and 25 healthy controls further completed social cognition (empathy and theory of mind) tasks. The results showed that the glutamate and glutamine levels did not differ between patients with schizophrenia and healthy controls. However, the glutamine level was negatively correlated with the score of cognitive theory of mind in schizophrenia patients, while the glutamine level was negatively correlated with affective empathy score in healthy controls.
Study 2 examined the glutamate level in anterior cingulate cortex and its correlation with social cognition in 36 participants with high level of schizotypy and 35 participants with low level of schizotypy. All participants completed social cognition (empathy and theory of mind) tasks. The results showed that the glutamate levels did not differ between participants with high and low levels of schizotypy.
However, the glutamate level was negatively correlated with the score of cognitive theory of mind in participants with high level of schizotypy, while there was no significant correlation between glutamate level and social cognition in participants with low level of schizotypy.
In conclusion, the present findings suggested there were negative correlations between the glutamate level in anterior cingulate cortex and cognitive theory of mind in both patients with schizophrenia and individuals with high level of schizotypy. These findings support the role of glutamatergic system in social cognition in both patients with schizophrenia and individuals with high level of schizotypy.
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