A kynurenine pathway enzyme aminocarboxymuconate-semialdehyde decarboxylase may be involved in treatment-resistant depression, and baseline inflammation status of patients predicts treatment response: a pilot study.

The kynurenine pathway (KP) and inflammation are substantial in depression pathogenesis. Although there is a crosstalk between the KP, inflammation, and neurotrophic factors, few studies examine these topics together. Novel medications may be developed by clarifying dysregulations related to inflammation, KP, and neurotrophic factors in treatment-resistant depression (TRD). We aimed to evaluate the serum levels of KP metabolites, proinflammatory biomarkers, and brain-derived neurotrophic factor (BDNF) in healthy controls (HC) and the patients with TRD whose followed up with three different treatments. Moreover, the effect of electroconvulsive therapy (ECT) and repetitive transcranial magnetic stimulation (rTMS) on biomarkers was investigated. Study groups comprised a total of 30 unipolar TRD patients consisting of three separate patient groups (ECT = 8, rTMS = 10, pharmacotherapy = 12), and 9 HC. The decision to administer only pharmacotherapy or ECT/rTMS besides pharmacotherapy was given independently of this research by psychiatrists. Blood samples and symptom scores were obtained three times for patients. At baseline, quinolinic acid (QUIN) was higher in the patients with TRD compared to HC, whereas picolinic acid (PIC), PIC/QUIN, and PIC/3-hydroxykynurenine were lower. Baseline interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hsCRP) were higher in nonresponders and non-remitters. ECT had an acute effect on cytokines. In the rTMS group, tumor necrosis factor-α (TNF-α) decreased in time. PIC, QUIN, and aminocarboxymuconate-semialdehyde decarboxylase (ACMSD) enzyme may play a role in TRD pathogenesis, and have diagnostic potential. rTMS and ECT have modulatory effects on low-grade inflammation seen in TRD. Baseline inflammation severity is predictive in terms of response and remission in depression.

1H-magnetic resonance spectroscopy in first episode and chronic schizophrenia patients.

BACKGROUND/AIM: The aim of this study was to compare metabolite levels of the dorsolateral prefrontal cortex (DLPFC), anterior cingulate gyrus (ACG), thalamus, and hippocampus in patients with chronic schizophrenia (CSPs) and first psychotic episode patients (FEPs) by the use of magnetic resonance spectroscopy (MRS). MATERIALS AND METHODS: Thirty CSPs, 20 FEPs, and 30 healthy subjects participated in this study. N-Acetylaspartate (NAA), creatine, choline (Cho), and myoinositol levels of the DLPFC, ACG, thalamus, and hippocampus were measured by 1H-MRS. RESULTS: It was determined that the NAA/Cho ratio was lower in both the FEPs and CSPs than the healthy controls in the DLPFC. DLPFC Cho levels were also higher in CSPs than healthy controls. NAA levels in CSPs were significantly lower than in the control group in the hippocampus. There was no significant difference in neurometabolite levels and ratios in the ACG and thalamus between the groups. CONCLUSION: This study supports neuronal dysfunction or loss of neuronal integrity in the DLPFC and hippocampus in CSPs. FEPs showed less neuronal dysfunction in the DLPFC, but not in the hippocampus. Our results suggest that schizophrenic patients show brain metabolic changes with the onset of the disorder in the DLPFC; these changes could be more apparent in the hippocampus as the disease progresses to chronic stages.