Schizophrenia is a debilitating mental disorder with complex etiology. Early identification of high-risk individuals and early intervention for early-stage patients can help improve prognosis, but effective identification methods are lacking. In recent years, research on proteomic techniques based on peripheral blood has achieved certain advancements in exploring the etiology of schizophrenia, as well as in early recognition and diagnostic modeling. This paper provides a review of the research methodologies of peripheral blood-based proteomics and the candidate biomarkers identified through these method.

The patient was a 25-year-old male who initially presented with emotional issues and later developed involuntary movements following the use of antipsychotic and antidepressant medications. He was initially misdiagnosed with Tardive Dyskinesia, a condition commonly associated with psychotropic drugs. However, due to the severity of his involuntary movements, the ineffectiveness of treatment, and a notable family history, genetic testing was performed. The test indicated a mutation in the VPS13A gene of the patient, and provided evidence for a final diagnosis of Chorea Acanthocytosis. This case report aims to enhance the recognition of movement disorders among psychiatrists and facilitate earlier identification of neurological diseases whose primary manifestation is involuntary movement.

Brain imaging abnormalities are present in schizophrenia (SZ) and bipolar disorder (BD), demonstrating disease-specific changes, yet they also share similarities in certain brain regions or functional characteristics, with SZ potentially exhibiting more extensive brain damage compared to BD. Structural magnetic resonance imaging (MRI) studies demonstrated widespread gray matter reductions in SZ, particularly in the prefrontal and temporal lobes. In BD, gray matter thickening was observed in the prefrontal lobes during manic episodes, while a reduction in gray matter was noted in the amygdala and hippocampus during depressive episodes. Both SZ and BD exhibited increased ventricular volume and reduced overall brain volume. Functional MRI studies revealed reduced functional connectivity in the prefrontal and temporal lobes in SZ, with decreased global and local efficiency in brain regions such as the hippocampus and cingulate gyrus. BD showed enhanced connectivity in the anterior cingulate gyrus and the default mode network (DMN). Both SZ and BD demonstrated altered functional connectivity in areas such as the striatum, salience network, central executive network and DMN. Diffusion tensor imaging studies showed decreased fractional anisotropy (FA) in the corpus callosum of SZ, with a decrease in FA in the left fronto-occipital fasciculus in BD. Both SZ and BD exhibited reduced FA in the uncinate fasciculus and corpus callosum. Magnetic resonance spectroscopy revealed decreased concentrations of glutathione, N-acetylaspartate (NAA) and inositol in the anterior cingulate gyrus of SZ. In BD, glutathione and inositol concentrations were elevated in the anterior cingulate gyrus, while NAA levels decreased during depressive episodes and increased during remission. Both SZ and BD showed increased levels of glutamate and gamma-aminobutyric acid in the prefrontal cortex. This article provides a review of the current evidence on the differences and similarities in multimodal magnetic resonance brain imaging between SZ and BD, aiming to offer a reference for future exploration of neuroimaging biomarkers and the neurobiological mechanisms of SZ and BD.

Brain imaging abnormalities are present in schizophrenia (SZ) and bipolar disorder (BD), demonstrating disease-specific changes, yet they also share similarities in certain brain regions or functional characteristics, with SZ potentially exhibiting more extensive brain damage compared to BD. Structural magnetic resonance imaging (MRI) studies demonstrated widespread gray matter reductions in SZ, particularly in the prefrontal and temporal lobes. In BD, gray matter thickening was observed in the prefrontal lobes during manic episodes, while a reduction in gray matter was noted in the amygdala and hippocampus during depressive episodes. Both SZ and BD exhibited increased ventricular volume and reduced overall brain volume. Functional MRI studies revealed reduced functional connectivity in the prefrontal and temporal lobes in SZ, with decreased global and local efficiency in brain regions such as the hippocampus and cingulate gyrus. BD showed enhanced connectivity in the anterior cingulate gyrus and the default mode network (DMN). Both SZ and BD demonstrated altered functional connectivity in areas such as the striatum, salience network, central executive network and DMN. Diffusion tensor imaging studies showed decreased fractional anisotropy (FA) in the corpus callosum of SZ, with a decrease in FA in the left fronto-occipital fasciculus in BD. Both SZ and BD exhibited reduced FA in the uncinate fasciculus and corpus callosum. Magnetic resonance spectroscopy revealed decreased concentrations of glutathione, N-acetylaspartate (NAA) and inositol in the anterior cingulate gyrus of SZ. In BD, glutathione and inositol concentrations were elevated in the anterior cingulate gyrus, while NAA levels decreased during depressive episodes and increased during remission. Both SZ and BD showed increased levels of glutamate and gamma-aminobutyric acid in the prefrontal cortex. This article provides a review of the current evidence on the differences and similarities in multimodal magnetic resonance brain imaging between SZ and BD, aiming to offer a reference for future exploration of neuroimaging biomarkers and the neurobiological mechanisms of SZ and BD.

Schizophrenia is a debilitating mental disorder with complex etiology. Early identification of high-risk individuals and early intervention for early-stage patients can help improve prognosis, but effective identification methods are lacking. In recent years, research on proteomic techniques based on peripheral blood has achieved certain advancements in exploring the etiology of schizophrenia, as well as in early recognition and diagnostic modeling. This paper provides a review of the research methodologies of peripheral blood-based proteomics and the candidate biomarkers identified through these method.

The patient was a 25-year-old male who initially presented with emotional issues and later developed involuntary movements following the use of antipsychotic and antidepressant medications. He was initially misdiagnosed with Tardive Dyskinesia, a condition commonly associated with psychotropic drugs. However, due to the severity of his involuntary movements, the ineffectiveness of treatment, and a notable family history, genetic testing was performed. The test indicated a mutation in the VPS13A gene of the patient, and provided evidence for a final diagnosis of Chorea Acanthocytosis. This case report aims to enhance the recognition of movement disorders among psychiatrists and facilitate earlier identification of neurological diseases whose primary manifestation is involuntary movement.

Negative symptoms of schizophrenia profoundly affect patients' social function and life quality, and traditional treatments have limited efficacy in improving these symptoms. In recent years, non-invasive brain stimulation techniques such as repetitive transcranial magnetic stimulation (rTMS), transcranial direct current stimulation (tDCS), transcranial alternating current stimulation (tACS), and transcranial random noise stimulation (tRNS) have shown potentiality in alleviating negative symptoms. However, the selection of stimulation targets remains an area of active research, as different targets may yield varying therapeutic outcomes. Therefore, identifying the most appropriate treatment targets is crucial for improving negative symptoms. This article reviews the targets selection and therapeutic effects of different non-invasive brain stimulation techniques for ameliorating negative symptoms, to provide guidance for target selection in clinical treatment.

Objective:To investigate the efficacy and safety of high-precision transcranial direct current stimulation (tDCS) targeting the anterior prefrontal cortex (aPFC) in prospective memory (PM) deficits in patients with schizophrenia.Methods:A total of 38 schizophrenia patients with PM deficits admitted to Outpatient Department of Psychiatry, Beijing Anding Hospital Affiliated to Capital Medical University from March 2022 to March 2023 were included and divided into true stimulus group ( n=19) and pseudo-stimulus group ( n=19) by random envelope method. Two mA stimulation current intensity with duration of 20 min was given to the true stimulus group, and same stimulation current intensity with duration of 40 s was given to the pseudo-stimulus group twice daily for 5 d. PM function was assessed by Cued Unfocused Laboratory Prospective Memory Task before and 1 week after stimulation, cognitive function and severity of clinical symptoms were evaluated by Positive and Negative Symptom Scale (PANSS) and Chinese version of MATRICS consensus cognition test (MCCB). Safety was assessed by tDCS adverse reaction questionnaire at the end of stimulation. Results:The time (before and 1 week after stimulation) and group interactions of PM trial accuracy and PM trial response time between the two groups were not significantly different ( P>0.05). Compared with that before stimulation, the PM trial accuracy 1 week after stimulation was significantly improved in the true stimulus group ([0.38±0.22] % vs. [0.57±0.28] %, P<0.05). No significant difference in PM trial accuracy ([0.56±0.25] % vs. [0.67±0.25] %) or PM trial response time ([2 216.46±570.03] ms vs. [2 059.59±378.41] ms) between before and 1 week after stimulation was noted in the pseudo-stimulus group ( P>0.05). In terms of severity of clinical symptoms and cognitive function, no significant difference in PANSS or MCCB scores were noted between the true stimulus group and pseudo-stimulus group 1 week after treatment ( P>0.05); no significant difference was noted between the two groups in time (before and 1 week after stimulation) and group interaction of all indexes ( P>0.05). In terms of adverse reactions, compared with the pseudo-stimulus group, the true stimulus group had significantly higher score of "skin redness" ( P<0.05); no significant differences in scores of other adverse reactions were noted between the two groups ( P>0.05). No serious adverse events occurred in all patients. Conclusion:In this study, no positive results have been found in improving PM deficits in patients with schizophrenia with high-precision tDCS targeting aPFC, but existing results suggest an improved trend, which can provide preliminary evidence for subsequent large-sample clinical trials to improve PM deficits in schizophrenia.

AIM:To investigate the therapeutic effects of chrysin on nonalcoholic steatohepatitis(NASH).METHODS:Eight-week-old male C57BL/6 mice were randomly divided into control group,model group,and chrysin group.The mice in control group were fed with normal diet,and those in model and chrysin groups were fed with methio-nine-and choline-deficient(MCD)diet.After 5 weeks of adaptation,the mice in chrysin group received chrysin treatment(20 mg/kg)by continuous lavage for 6 weeks,while those in control and model groups were given equal volume of saline.During the experiment,the health condition of the mice was monitored.Liver morphology was examined after the mice were sacrificed.Serum triglyceride(TG),total cholesterol(TC),low-density lipoprotein cholesterol(LDL-C),high-den-sity lipoprotein cholesterol(HDL-C),alanine aminotransferase(ALT)and aspartate aminotransferase(AST)levels were measured using a biochemical analyzer.Liver tissue TG and TC levels were measured using assay kits.Liver cell damage and inflammation were assessed by hematoxylin-eosin(HE)staining and F4/80 immunohistochemistry staining.The ex-tent of liver lipid deposition was explored by oil red O staining.Masson staining and Sirius red staining were performed to assess liver fibrosis.Immunohistochemistry was performed to analyze the expression of fibrosis-related molecules.RE-SULTS:Compared with control group,the mice in model group showed significant decrease in body weight,liver wet weight,and liver volume.Serum TG,LDL-C,ALT and AST levels,as well as liver TG and TC levels were significantly elevated,and HDL-C levels were decreased in model group.Pathological staining showed significant inflammatory cell in-filtration,lipid deposition,and liver fibrosis.After the treatment with chrysin,increased body weight and liver weight,a reddish appearance of the liver,relatively smooth surface,and sharp liver edges were observed.Serum TG,LDL-C,AST and ALT levels,and liver TG levels were significantly reduced by chrysin.Inflammatory cell infiltration,lipid deposition,and liver tissue fibrosis were also significantly attenuated by chrysin.CONCLUSION:Chrysin shows a potential as a can-didate drug for the treatment of NASH by inhibiting hepatic steatosis,inflammation,and liver fibrosis.

Schizophrenia is a chronic disabling disease of unknown etiology. Its neuroimaging abnormalities have been confirmed by a large number of studies. However, when these structural abnormalities occur and how they develop over time are unclear. The relationship between structural abnormalities and antipsychotic treatment needs to be further explored. Longitudinal studies on the brain structure of clinical high risk for psychosis, first-episode schizophrenia and chronic schizophrenia, exploring the influence of drug therapy on them, are helpful to construct the trajectories of brain structure changes in the whole course of schizophrenia and dynamically track the brain structure changes, so as to further explore the pathophysiology of schizophrenia. This article reviews the longitudinal research progress of brain structure changes in patients with schizophrenia.