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DNA methylation in the promoter region of the glucocorticoid receptor gene (NR3C1) is closely associated with childhood adversity and suicide. However, few studies have examined NR3C1 methylation in relation to major depressive disorder (MDD) and hippocampal subfield volumes. We investigated the possible association between NR3C1 methylation and structural brain alterations in MDD in comparison with healthy controls. We compared the degree of NR3C1 promoter methylation in the peripheral blood of non-psychotic outpatients with MDD and that of healthy controls. Correlations among NR3C1 promoter methylation, structural abnormalities in hippocampal subfield volumes and whole-brain cortical thickness, and clinical variables were also analyzed. In total, 117 participants (45 with MDD and 72 healthy controls) were recruited. Patients with MDD had significantly lower methylation than healthy controls at 2 CpG sites. In MDD, methylations had positive correlations with the bilateral cornu ammonis (CA) 2-3 and CA4-dentate gyrus (DG) subfields. However, in healthy controls, methylations had positive correlation with the subiculum and presubiculum. There were no differences in total and subfield volumes of the hippocampus between patients with MDD and healthy controls. Compared with healthy controls, patients with MDD had a significantly thinner cortex in the left rostromiddle frontal, right lateral orbitofrontal, and right pars triangularis areas. Lower methylation in the NR3C1 promoter, which might have compensatory effects relating to CA2-3 and CA4-DG, is a distinct epigenetic characteristic in non-psychotic outpatients with MDD. Future studies with a longitudinal design and a comprehensive neurobiological approach are warranted in order to elucidate the effects of NR3C1 methylation.

Background: We performed a meta-analysis in order to determine which neuropsychological domains and tasks would be most sensitive for discriminating between patients with major depressive disorder (MDD) and healthy controls. Methods: Relevant articles were identified through a literature search of the PubMed and Cochrane Library databases for the period between January 1997 and May 2011. A meta-analysis was conducted using the standardized means of individual cognitive tests in each domain. The heterogeneity was assessed, and subgroup analyses according to age and medication status were performed to explore the sources of heterogeneity. Results: A total of 22 trials involving 955 MDD patients and 7,664 healthy participants were selected for our meta-analysis. MDD patients showed significantly impaired results compared with healthy participants on the Digit Span and Continuous Performance Test in the attention domain; the Trail Making Test A (TMT-A) and the Digit Symbol Test in the processing speed domain; the Stroop Test, the Wisconsin Card Sorting Test, and Verbal Fluency in the executive function domain; and immediate verbal memory in the memory domain. The Finger Tapping Task, TMT-B, delayed verbal memory, and immediate and delayed visual memory failed to separate MDD patients from healthy controls. The results of subgroup analysis showed that performance of Verbal Fluency was significantly impaired in younger depressed patients (<60 years), and immediate visual memory was significantly reduced in depressed patients using antidepressants. Conclusions: Our findings have inevitable limitations arising from methodological issues inherent in the meta-analysis and we could not explain high heterogeneity between studies. Despite such limitations, current study has the strength of being the first meta-analysis which tried to specify cognitive function of depressed patients compared with healthy participants. And our findings may provide clinicians with further evidences that some cognitive tests in specific cognitive domains have sensitivity to discriminate MDD patients from healthy controls.

The aim of this study was to evaluate the relationship of serum reproductive hormone levels with cognitive function and negative symptoms in schizophrenic women during the follicular phase of the menstrual cycle. Thirty-five women with chronic schizophrenia who had minimal positive symptoms participated in this study. We evaluated the correlation of serum reproductive hormone levels with the Scale for the Assessment of Negative Symptoms (SANS) and cognitive function tests such as the Immediate Visual Recognition Scale, Oral Fluency Test, List Recall Scale with List Acquisition Scale, Trail Making Tests A and B, and Digit Symbol Test. The patients were divided into two subgroups (low estradiol group and normal estradiol group) using the normal serum reference range for estradiol. Significant correlation between SANS subcategories, such as Alogia and Attention Impairment, and estradiol were found. Moreover, significant relationships between the estradiol level and the Oral Fluency Test, List Recall Scale with List Acquisition Scale, Trail Making Test B and Digit Symbol Test were observed. In the low estradiol group, the SANS scores, except for Anhedonia-Asociality and Avolition-Apathy, were significantly higher than those in the normal estradiol group. Patients in the low estradiol group had a significantly lower performance in the cognitive function tests, except Visual Recognition Scale, when compared to patients in the normal estradiol group. These results suggest that for schizophrenic women of reproductive age, lower levels of estrogen are associated with more severe negative symptomatology as well as reduced performance in cognitive function, especially verbal performance and executive functioning.

Background: Alexithymia is a condition characterized by deficits in cognitive processing and the regulation of emotions. Several theories have been proposed for the underlying neurobiology, but the etiology of alexithymia remains unclear. Methods: Using functional magnetic resonance imaging, we investigated brain activation measured on the scale of alexithymia in 38 individuals who were presented with neutral, sad, or angry affective facial stimuli. Results: We found significant inverse correlations between the degree of alexithymia represented by the Korean version of the Toronto Alexithymia Scale (TAS-20K) and the intensity of the neural response to angry facial stimuli over neutral facial stimuli in the right caudate. This result was mainly due to the activations in factor 2 (difficulty describing feelings) in TAS-20K scale. Conclusions: The results suggest that functional impairments in the caudate of the fronto-striatal circuitry may play important roles in the pathophysiology of alexithymia.

About 2% to 5% of all primary-care patients have a somatization disorder, and somatic symptoms are strongly associated with comorbid depression and anxiety disorders. The authors evaluated the validity of the 15-item Somatization module of the Patient Health Questionnaire (PHQ–15) among psychiatric outpatients. The PHQ–15 was administered to patients with somatic complaints; it was compared with the Beck Depression Inventory (BDI) and the General Health Questionnaire–12 (GHQ–12). Fifty-seven Korean subjects completed the survey. The PHQ–15 exhibited significant internal consistency, and test–retest reliability. Convergent validity with the BDI and GHQ–12 were positive. These results indicate that the Korean version of the PHQ–15 is appropriate for measuring the severity of somatic symptoms in a psychiatric outpatient setting.

Background/Aims: It has been suggested that the serotonergic systems are associated with anger and aggressive behaviors. We investigated the association between several single nucleotide polymorphisms in the serotonergic genes and anger-related personality traits. Methods: A total of 228 healthy female Korean women participated in this study. All subjects were assessed with the State-Trait Anger Expression Inventory (STAXI) and were genotyped for 3 polymorphisms: serotonin transporter (5-HTT) gene-linked polymorphic region (5-HTTLPR), tryptophan hydroxylase 1 (TPH1) A218C, and TPH2 G-703T. Results: The Anger Expression-Out (AX-Out) subscale scores of the STAXI differed significantly between the genotypes for the TPH2 G-703T polymorphism (F = 4.825, p = 0.009). G/G homozygous subjects scored significantly higher on the AX-Out subscale than those with the G/T genotype. However, no significant differences were observed in the relationships between the STAXI subscale scores of subjects with other polymorphisms. Conclusions: This study suggests that the TPH2 G-703T polymorphism might contribute to anger-related traits, especially to the expression of anger.

Objective: The cause of restless legs syndrome (RLS) is not yet clear, but more promising theories involve dopaminergic deficiency and genetic causes. This study investigated whether single-nucleotide polymorphisms in the genes of dopamine receptors DRD1, DRD2, DRD3 and DRD4 are associated with antipsychotics-induced RLS in schizophrenia. Methods: We evaluated 190 Korean schizophrenic patients using the diagnostic criteria of the International Restless Legs Syndrome Study Group and its rating scale for RLS. Genotyping was performed for the DRD1 gene –48A/G, DRD2 gene TaqI A, DRD3 gene Ser9Gly and DRD4 gene –521C/T single-nucleotide polymorphisms. The method of multifactor dimensionality reduction was used to analyze gene-gene interactions. Results: We classified the schizophrenic patients into 96 with and 94 without RLS symptoms. The genotype frequencies of all polymorphisms investigated did not differ significantly between these 2 groups. MDR analysis did not show a significant effect of the 4 dopamine receptor gene variants on susceptibility to antipsychotic-induced RLS symptoms (p > 0.05). Conclusions: These genetics data suggest that the analyzed polymorphisms of the dopamine genes may not be associated with RLS symptoms in schizophrenia. Confirming the results reported here requires a larger-scale study involving patients taking specific antipsychotics.

We evaluated plasma levels of DHEA-S and cortisol before and after treating ADHD patients with one of two medications: methylphenidate ( n  = 12) or bupropion ( n  = 10). Boys with ADHD (combined type) were evaluated with the Korean ADHD rating scale (K-ARS) and the computerized ADHD diagnostic system (ADS). All assessments were measured at baseline and repeated after 12 weeks. There were significant clinical improvements in both treatment groups as measured by K-ARS and ADS. DHEA-S levels increased from baseline to endpoint, but cortisol levels did not change significantly. This study suggests that both methylphenidate and bupropion increase plasma levels of DHEA-S in boys with ADHD.

Tardive dyskinesia (TD) is a long-term adverse effect of antipsychotics. We evaluated whether a candidate functional polymorphism of the dopamine D4 receptor (DRD4) gene is associated with drug-induced TD in 209 Korean schizophrenic patients with TD (n = 83) and without TD (n = 126) who were matched for antipsychotic drug exposure and other relevant variables. There was no significant association of the genotype and allele frequencies determined by the –521 C/T SNP of DRD4 between TD and non-TD patients. In addition, there was no significant difference in terms of total Abnormal Involuntary Movement Scale scores among the 3 genotype groups. Within the limitations imposed by the size of the clinical sample, these findings suggest that the DRD4 –521 C/T SNP does not contribute significantly to the risk for TD.

Objective: This study investigated whether the catechol-O-methyltransferase (COMT) gene V158M single-nucleotide polymorphism (SNP) influences susceptibility to tardive dyskinesia (TD). Methods: We examined 209 Korean schizophrenic patients using the Abnormal Involuntary Movement Scale (AIMS), with genotyping performed for the COMT gene V158M SNP. Results: The logistic regression analysis showed that old age [p = 0.032, OR = 1.40 (OR corresponds to 10-year), 95% CI = 1.03–1.90] was a risk factor for TD, but there was no significant association between the COMT genotype and TD. The heterozygotes (MV genotype) of the COMT gene polymorphism tended to develop TD less than homozygotes (MM and VV); however, the risk did not reach statistical significance (p = 0.050, OR = 1.81, 95% CI = 1.00–3.29). Conclusions: These results suggest that the V158M SNP of the COMT gene is not associated with TD in schizophrenia. However, there is a tendency that the heterozygous genotype of the COMT gene polymorphism has a protective effect against TD. Further investigations are warranted to evaluate a molecular heterosis of this polymorphism in development of TD in a large sample of subjects.