RESUMO
Background: Several hypotheses regarding the pathomechanisms of schizophrenia have been proposed. If schizophrenia is a unitary disease, then these pathological processes must be linked; however, if such links do not exist, schizophrenia may best be considered a group of disorders. Only a few studies have examined the relationships among these pathomechanisms. Herein, we examined the relationships among deficient myelination, NMDA receptor hypofunction, and metabolic dysregulation by measuring various plasma markers and examining their correlations. Methods: Plasma samples were collected from 90 patients with schizophrenia and 68 healthy controls. Concentrations of nardilysin (N-arginine dibasic convertase, NRDC), a positive regulator of myelination, the NMDA receptor co-agonist d-serine and glycine, various additional amino acids related to NMDA receptor transmission (glutamate, glutamine, and l-serine), and homocysteine (Hcy), were measured. Concentrations were compared using independent samples t-test or logistic regression, and associations were evaluated using Pearson's correlation coefficients. Results: Plasma glycine (t = 2.05, p = 0.042), l-serine (t = 2.25, p = 0.027), and homocysteine (t = 3.71, p < 0.001) concentrations were significantly higher in patients with schizophrenia compared to those in healthy controls. Logistic regression models using age, sex, smoking status, glutamine, glutamate, glycine, l-serine, d-serine, homocysteine, and NRDC as independent variables revealed significantly lower plasma d-serine (p = 0.024) and NRDC (p = 0.028), but significantly higher l-serine (p = 0.024) and homocysteine (p = 0.001) in patients with schizophrenia. Several unique correlations were found between NMDA receptor-related amino acids and NRDC in patients with schizophrenia compared to those in healthy controls, while no correlations were found between plasma homocysteine and other markers. No associations were found between plasma marker concentrations and disease status or cognitive function in patients with schizophrenia, except for a significant correlation between plasma glycine and full intelligence quotient. Conclusion: Reduced myelination and NMDA receptor hypofunction may be related to pathological mechanisms in schizophrenia, while homocysteine dysregulation appears to be an independent pathological process. These results suggest that schizophrenia may be a group of disorders with unique or partially overlapping etiologies.
RESUMO
Background: Lack of social support is associated with depression, anxiety, and insomnia. This study aimed to determine the source of support related to depression, anxiety, and insomnia among Japanese workers. Methods: As part of a cohort study, we conducted a questionnaire survey among city government employees in Koka City, Shiga Prefecture, Japan, from September 2021 to March 2022. We used the Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder-7 (GAD-7), and Insomnia Severity Index (ISI) to assess depressive symptoms, anxiety symptoms, and insomnia, respectively. We used the Brief Job Stress Questionnaire (BJSQ) to assess job stressors and social support (from supervisors, colleagues, and family). Results: A total of 1,852 Japanese employees (38.4% male, 45.9 ± 12.9 years) participated in the survey, with 15.5, 10.8, and 8.2% of the participants having depressive symptoms (PHQ-9 ≥ 10), anxiety symptoms (GAD-7 ≥ 10), and insomnia (ISI ≥ 15), respectively. The logistic regression analysis suggested that job stressors were associated with depressive symptoms (p < 0.001), anxiety symptoms (p < 0.001), and insomnia (p = 0.009). In contrast, support from co-workers (p = 0.016) and family members (p = 0.001) was associated with decreased depressive symptoms. Support from family members was associated with decreased insomnia (p = 0.005). Conclusion: Social support from co-workers and family may be associated with reduced depressive symptoms, and family support may be associated with reduced insomnia in the Japanese working population. Clinical trial registration: https://clinicaltrials.gov/ct2/show/NCT03276585.
