Alexithymia is associated with insomnia in Chinese patients with schizophrenia.

Background: Sleep disorders are prevalent among patients with schizophrenia and are associated with several negative consequences. Although, researchers have recently suggested that sleep disorders have a close correlation with alexithymia, and schizophrenia also has a strong correlation with alexithymia, there have been few studies on the relationships between schizophrenia, sleep disorders and alexithymia. Therefore, this study aimed to explore the relationships between psychiatric symptoms, alexithymia and sleep problems in patients with schizophrenia so as to provide a reference for the clinical treatment of this comorbidity. Methods: In total, 977 patients with schizophrenia were recruited for this study. The Insomnia Severity Index (ISI) was used to assess sleep disorders, and the Positive and Negative Syndrome Scale (PANSS), Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) and Toronto Alexithymia Scale (TAS) were used to evaluate clinical symptoms, cognitive functions and the ability to express emotion, respectively. Results: The results indicated that the PANSS subscales (G-subscore) and TAS group were risk factors for insomnia in schizophrenia patients (all p < 0.05). The mediation model showed the standardized path coefficients from schizophrenia to alexithymia (ß = 0.104, p < 0.001) and from alexithymia to insomnia (ß = 0.038, p < 0.001) were statistically significant. Conclusion: The results of this study indicated that alexithymia is associated with sleep disturbance in patients with schizophrenia. These findings may provide a new avenue for the treatment of schizophrenia patients with sleep disorders.

Obesity Exacerbates Rat Cerebral Ischemic Injury through Enhancing Ischemic Adiponectin-Containing Neuronal Apoptosis.

A diet consisting of high levels of saturated fat has been linked to a dramatic rise in obesity. Long-term exposure to high fat, "Western diet" (WD), is detrimental to ischemic brain injury. Adiponectin receptor 1 (ADR-1) activation is also shown to exacerbate ischemic neuronal death. However, it is not known whether increasing percentages of adiponectin (APN)-containing neurons attenuates ischemic neuronal apoptosis by modulating ADRS. To explore the role of APN and its ADRs in the development of acute cerebral injury, we subjected WD and control diet (CD) rats to 1 h of middle cerebral artery occlusion followed by 23 h of reperfusion. Compared with CD rats, WD rats exhibited higher levels of brain infarct, neurologic deficits, brain edema, and apoptosis of APN-containing neurons; upregulation of both ADR-1 and P38 mitogen-activated protein kinase (P38MAPK); and downregulation of ADR-2 in ischemic brain tissues including frontal cortex, striatum, and hippocampus. Increasing percentages of APN-containing neurons by baculovirus-mediated administration of APN, in addition to reducing apoptosis of APN-containing neurons in ischemic brain tissues, significantly attenuated brain infarct and edema, neurologic deficits, and altered expression of ADR-1, P38MAPK, and ADR-2 in both WD and CD group rats. These data suggest a negative correlation between percentages of APN-containing neurons and cerebral ischemic injury. Obesity could exacerbate rat cerebral ischemic injury by enhancing apoptosis of APN-containing neurons in ischemic brain tissues probably via modulating ADRs and P38MAPK.

Inhibition of Peripheral TNF-α and Downregulation of Microglial Activation by Alpha-Lipoic Acid and Etanercept Protect Rat Brain Against Ischemic Stroke.

Ischemic stroke, caused by obstruction of blood flow to the brain, would initiate microglia activation which contributes to neuronal damage. Therefore, inhibition of microglia-mediated neuroinflammation could be a therapeutic strategy for ischemic stroke. This study was aimed to elucidate the anti-inflammatory effects of alpha-lipoic acid and etanercept given either singly or in combination in rats subjected to middle cerebral artery occlusion. Both α-lipoic acid and etanercept markedly reduced cerebral infarct, blood-brain barrier disruption, and neurological motor deficits with the former drug being more effective with the dosage used. Furthermore, when used in combination, the reduction was more substantial. Remarkably, a greater diminution in the serum levels of tumor necrosis factor-alpha as well as the brain levels of microglial activation (e.g., microgliosis, amoeboid microglia, and microglial overexpression of tumor necrosis factor-α) was observed with the combined drug treatment as compared to the drugs given separately. We conclude that inhibition of peripheral tumor necrosis factor-alpha as well as downregulation of brain microglial activation by alpha-lipoic acid or etanercept protect rat brain against ischemic stroke. Moreover, when both drugs were used in combination, the stroke recovery was promoted more extensively.