Gray Matter Volume Reductions Were Associated with TPH1 Polymorphisms in Depressive Disorder Patients with Suicidal Attempts

OBJECTIVE: Structural changes of brain areas have been reported in depressive disorder and suicidal behavior (SB), in which TPH1 also has been known as a promising candidate gene. We investigated gray matter volume (GMV) differences, TPH1 rs1800532 and rs1799913 polymorphisms previously found to be associated with depressive disorder and SB, and the relationship between the two markers. METHODS: Thirteen depressive disorder patients with suicidal attempts (SA) and twenty healthy controls were included. We examined GMV differences using a voxel-based morphometry and regions of interest analysis. Direct sequencing was used for genotyping. RESULTS: The patients showed significant GMV reduction in left cerebral region including middle frontal gyrus, inferior frontal gyrus, and anterior cingulate cortex; in right middle temporal gyrus; in left cerebellar tonsil; and in right cerebral region including precentral gyrus and postcentral gyrus (corrected p < 0.005). The right precentral and postcentral gyri GMV values of AA and CA genotypes patients were significantly decreased compared to those of CC genotype subjects (corrected p=0.040). CONCLUSION: These findings show the possibility that both GMV reductions and TPH1 rs1800532/rs1799913 A allele may be involved in the pathogenesis of depressive disorder patients with SA.

Association of Therapeutic Response and Change of Mismatch Negativity in Schizophrenia Patients

OBJECTIVES: Schizophrenia is characterized by disturbances in perception and cognition. Attenuated mismatch negativity (MMN) reflects central auditory dysfunction in schizophrenia. The aim of this study is to compare MMN changes before and after treatment in schizophrenia patients and to assess their association with treatment response. METHODS: Twenty-three schizophrenia patients underwent an oddball paradigm. MMN was calculated by the difference waveforms of the event-related potentials (ERPs) elicited by subtracting standard from deviant stimulus. The clinical symptoms were measured by the Positive and Negative Syndrome Scale (PANSS), the Psychotic Symptom Rating Scale (PSYRATS). Follow-up evaluation was conducted when the PANSS total score decreased by 30% or more (treatment response group) or before discharge (non-response group). RESULTS: The treatment response group showed significantly larger MMN amplitude improvement and latency reduction than the non-response group after treatment (Fz ; mean amplitude p = 0.035, FCz ; p = 0.041). The auditory hallucination group showed shorter latency than that of the group without hallucinations. Additionally, auditory hallucination was associated with prolonged MMN latency and shortened after treatment in the auditory hallucination response group (Fz ; p = 0.048). CONCLUSIONS: These results suggest that the attenuated MMN amplitude reflects the progression of the disease. The increment of MMN amplitude and shortening of latency after treatment may reflect cognitive functional recovery of central auditory sensory processing.