ABSTRACT
Objective To explore the effects of aripiprazole on clinical symptoms and neurotrophic factor levels in patients with schizophrenia. Methods Forty patients with schizophrenia and 40 normal controls were included in the study. The clinical symptoms of patients receiving aripiprazole only for 12 weeks were evaluated by using the Positive and Negative Syndrome Scale (PANSS). Stroop Color-Word Test (SCWT), Continuous Performance Test, Digit-Symbol Coding Test and Trail Making Test-A were used to evaluate the cognitive function both in patients and controls. Serum levels of Nerve Growth Factor (NGF), Brain Derived Neurotrophic Factor (BDNF) and Neurotrophin 3 (NT-3) were measured using enzyme linked immunosorbent assay. Results The clinical scores, cognitive function and levels of neurotrophic factors were different before and after treatment (P<0.01). And those were significantly lower in patients than in control group (P<0.05). Before treatment, BDNF was negatively correlated with PANSS negative symptom score (r=-0.362, P=0.022);NGF was related to the total score of PANSS (r=0.332, P=0.037) and positive symptoms (r=0.401, P=0.010); NT-3 was associated with negative symptom scores (r=-0.376, P=0.017) and SCWT-color words (r=0.332, P=0.037) in patient group. After treatment, the increase in BDNF was correlated with the reduction in PANSS total score (r=0.371, P=0.018), negative symptom score (r=0.345, P=0.029) and general pathology score (r=0.342, P=0.031). There was a correlation of the increase of NGF with the decrease of PANSS total scores (r=0.437, P=0.005) and with positive symptom scores (r=0.357, P=0.024). Conclusion Treatment with Aripiprazole can improve the clinical symptoms and cognitive functiona impairments in patients with schizophrenia, which may be related to the increase in serum levels of BDNF, NGF and NT-3.
ABSTRACT
Objective To investigate the effects of specific TrkB receptor agonist 7,8-dihydroxyflavone ( 7,8-DHF) on spatial cognitive function and synaptic structure in schizophrenia rat model. Methods SD infant rats were divided into normal control group and model group according to the random number table method on the 6th day after birth. During the postnatal day 7 to 11, rats in the normal control group received subcutaneous injection of 0.9% sodium chloride solution (1 mL·kg-1) twice daily, and the rats in the model group were injected with dizocilpine (0.1 mg·kg-1). Beginning on the postnatal day 60, model rats were randomly divided into 7,8-DHF group and model control group, which were given intraperitoneal injection of 7,8-DHF ( 5 mg·kg-1 ) and DMSO once daily for 14 consecutive days, respectively. The rats of normal control group were given equal volume injections of DMSO. Morris water maze task, Golgi staining and Western blotting were adopted to examine spatial cognitive function, hippocampal dendritic spine density, protein expression and activity, respectively. Results The result in the open field test showed that the total travelled distance within 5 min was (12.20±1.62) m in the normal control group, (11.73±1.36) m in the model control group and (12.94±1.09) m in the 7,8-DHF group. The escape latency and travelled distance in the model control group were significantly higher than those in the normal control group (P<0.05), and the escape latency and travelled distance in rats of 7,8-DHF group were significantly shortened as compared with those in the model control group (P<0.05). There was no significant difference in the swimming speed among the three groups (P>0.05). The hippocampal dendritic spine density was (14.2±2.3)/10 μm in the normal control group, (8.0±1.9)/10 μm in the model control group, and (13.5±1.7)/10 μm in the 7,8-DHF group, the differences between the three groups were significant ( all P<0.05);the phosphorylation level of GluR1 protein was (100.0±5.0) in the normal control group, (47.9±10.8) in the model control group, and (97.5±9.3) in the 7,8-DHF group, and the differences among the three groups were significant ( all P<0. 05 ) . Conclusion 7, 8-DHF treatment could improve the spatial cognitive function in rat model of schizophrenia and the mechanisms might be related with the increases of hippocampal dendritic spine density and phosphorylated levels of GluR1.
ABSTRACT
Objective To investigate the effects of specific TrkB receptor agonist 7,8-dihydroxyflavone ( 7,8-DHF) on spatial cognitive function and synaptic structure in schizophrenia rat model. Methods SD infant rats were divided into normal control group and model group according to the random number table method on the 6th day after birth. During the postnatal day 7 to 11, rats in the normal control group received subcutaneous injection of 0.9% sodium chloride solution (1 mL·kg-1) twice daily, and the rats in the model group were injected with dizocilpine (0.1 mg·kg-1). Beginning on the postnatal day 60, model rats were randomly divided into 7,8-DHF group and model control group, which were given intraperitoneal injection of 7,8-DHF ( 5 mg·kg-1 ) and DMSO once daily for 14 consecutive days, respectively. The rats of normal control group were given equal volume injections of DMSO. Morris water maze task, Golgi staining and Western blotting were adopted to examine spatial cognitive function, hippocampal dendritic spine density, protein expression and activity, respectively. Results The result in the open field test showed that the total travelled distance within 5 min was (12.20±1.62) m in the normal control group, (11.73±1.36) m in the model control group and (12.94±1.09) m in the 7,8-DHF group. The escape latency and travelled distance in the model control group were significantly higher than those in the normal control group (P<0.05), and the escape latency and travelled distance in rats of 7,8-DHF group were significantly shortened as compared with those in the model control group (P<0.05). There was no significant difference in the swimming speed among the three groups (P>0.05). The hippocampal dendritic spine density was (14.2±2.3)/10 μm in the normal control group, (8.0±1.9)/10 μm in the model control group, and (13.5±1.7)/10 μm in the 7,8-DHF group, the differences between the three groups were significant ( all P<0.05);the phosphorylation level of GluR1 protein was (100.0±5.0) in the normal control group, (47.9±10.8) in the model control group, and (97.5±9.3) in the 7,8-DHF group, and the differences among the three groups were significant ( all P<0. 05 ) . Conclusion 7, 8-DHF treatment could improve the spatial cognitive function in rat model of schizophrenia and the mechanisms might be related with the increases of hippocampal dendritic spine density and phosphorylated levels of GluR1.
ABSTRACT
Objective To explore the change of serum insulin-like growth factor-2 (IGF-2) and its relationship with clinical characteristics in patients with schizophrenia. Methods Fifty-one schizophrenic patients were recruited in the present study and 50 healthy volunteers served as controls. The serum IGF-2 level was measured using enzyme linked immunosorbent assay (ELISA). Positive and Negative Syndrome Scale (PANSS) was used to evaluate the psychotic symp?toms of patients. Trail Making Test-A (TMTA), Digit-Symbol Coding Test (DSCT), Continuous Performance Test (CPT) and Stroop Color-Word Test (SCWT) were used to evaluate the cognitive function of both groups. Results There were sig?nificant differences in the results of TMTA, DSCT, CPT and SCWT between patient and control groups. The serum levels of IGF-2 were significantly lower in patients than that in controls [(202.7±40.7) ng/mL vs. (365.9±65.5) ng/mL, P0.05). Furthermore, significant correlations were found between the serum IGF-2 level and the negative symptom sub?scale of PANSS (r=-0.397, P=0.004), CPT score (r=0.378, P=0.006), SCWT-word number (r=0.289, P=0.040), SC? WT-color number (r=0.327, P=0.019) and SCWT-word/color number (r=0.386, P=0.005) in schizophrenic patients. Con?clusion The serum IGF-2 levels of patients with schizophrenia are significantly lower than that of healthy controls, and the IGF-2 level is associated with the severity of negative symptoms and cognitive impairments in patients, indicating that serum IGF-2 might be an indicator of the severity of schizophrenia.