Objective The existence of neuropsychological deficits has been implicated in obsessive-compulsive disorder （OCD）, particularly memory, attention, and executive functions. However, few studies have focused on neurop...Objective The existence of neuropsychological deficits has been implicated in obsessive-compulsive disorder （OCD）, particularly memory, attention, and executive functions. However, few studies have focused on neuropsychological deficits in the relatives of OCD patients. The aim of this study was to investigate cognitive deficits in OCD patients and their parents. Methods Forty patients with OCD, 48 parents of these patients, and 87 healthy controls completed a neuropsychological testing battery. Results Both OCD patients and their parents showed impairments in delayed verbal memory and delayed visual memory. Furthermore, they performed worse than healthy controls in problem-solving ability. Conclusion Our study demonstrated familial aggregation of delayed memory deficits and impaired problem-solving ability, which may be the potential neuropsychological endophenotypes of hereditary susceptibility to OCD.展开更多
The purpose of this study was to determine if the substituted pyrimidine, CXB-909 (formerly known as KP544) which has been shown to amplify the effects of nerve growth factor in elevating choline-acetyltransferase act...The purpose of this study was to determine if the substituted pyrimidine, CXB-909 (formerly known as KP544) which has been shown to amplify the effects of nerve growth factor in elevating choline-acetyltransferase activity in vitro, could attenuate memory deficits in the mu-p-75 saporin injected mouse model of Alzheimer’s disease (AD). Seventy-one, seven-week old C57/BL6 mice received daily oral intubation of 10, 15, or 20 mg/kg CXB-909, or vehicle (0.5% methylcellulose solution), which continued for 32 days. At postnatal week nine, mice received bilateral intra-cerebroventricular injections of mu-p-75 saporin, or sterile phosphate buffered saline. Seven days after surgery, mice were trained for two days, on a cued-platform version of the Morris water maze task, and then tested on a four-day hidden-platform version, followed by a one-day probe version of this task. Mice injected with mu-p-75 saporin, had increased latency to find the hidden-platform compared to sham mice. Furthermore, mice treated with CXB-909 at the 10, and 15 mg/kg doses, significantly reduced their latency to reach the hidden-platform, compared to vehicle-treated mice given mu-p-75 saporin. These results suggest that CXB-909 can attenuate memory deficits in the mu-p-75 saporin injected mouse model of AD.展开更多
目的探讨正常老年大鼠空间学习记忆能力变化与海马背侧组织胆固醇代谢之间的关系。方法实验大鼠分老年实验组和青年对照组,利用Morris水迷宫方法评价空间学习记忆能力,然后测定海马背侧组织胆固醇含量及代谢相关酶羟甲基戊二酸单酰CoA...目的探讨正常老年大鼠空间学习记忆能力变化与海马背侧组织胆固醇代谢之间的关系。方法实验大鼠分老年实验组和青年对照组,利用Morris水迷宫方法评价空间学习记忆能力,然后测定海马背侧组织胆固醇含量及代谢相关酶羟甲基戊二酸单酰CoA还原酶(3-hydroxy-3-methylglutaryl coenzyme A reductase,HMG-CoAR)和胆固醇-24S-羟化酶(cholesterol24-hydroxylase,CYP46)mRNA表达的变化。结果与青年对照组相比,老年实验组逃避潜伏期明显延长(P<0.05),海马背侧组织总胆固醇的含量明显升高(P<0.05),HMG-CoAR mRNA相对表达量无明显变化,CYP46mRNA相对表达量明显降低(P<0.05)。结论正常老年大鼠空间学习记忆能力下降可能与海马背侧组织胆固醇含量增加有关。展开更多
目的:观察中药健脑合剂对正常小鼠急性脑缺氧的保护作用及记忆障碍小鼠学习记忆的改善作用,并初步探讨其作用机理。方法:采用常压缺氧、亚硝酸钠缺氧及断头缺氧法观察健脑合剂对正常小鼠急性脑缺氧的保护作用;用跳台法、避暗法检测健脑...目的:观察中药健脑合剂对正常小鼠急性脑缺氧的保护作用及记忆障碍小鼠学习记忆的改善作用,并初步探讨其作用机理。方法:采用常压缺氧、亚硝酸钠缺氧及断头缺氧法观察健脑合剂对正常小鼠急性脑缺氧的保护作用;用跳台法、避暗法检测健脑合剂对由东莨菪碱、亚硝酸钠及乙醇所致记忆障碍小鼠的学习记忆能力的影响。结果:健脑合剂14g/kg 和28g/kg 对常压缺氧、亚酸钠缺氧及断头缺氧显示出显著延长急性脑缺氧状态下小鼠的生存时间的作用;同时显著增强小鼠被动学习能力,改善由东莨菪碱、亚硝酸钠及乙醇所致记忆获得、记忆巩固及记忆再现障碍。结论:中药健脑合剂对正常小鼠急性脑缺氧具有较好的保护作用并可改善记忆障碍模型小鼠学习记忆功能,其机制可能与提高大脑血氧水平、影响中枢 M 胆碱能系统等有关。展开更多
3′-Daidzein sulfonate sodium（DSS） is a new synthetic water-soluble compound derived from daidzein,a soya isoflavone that plays regulatory roles in neurobiology.In this study,we hypothesized that the regulatory role...3′-Daidzein sulfonate sodium（DSS） is a new synthetic water-soluble compound derived from daidzein,a soya isoflavone that plays regulatory roles in neurobiology.In this study,we hypothesized that the regulatory role of DSS in neurobiology exhibits therapeutic effects on hippocampal damage and memory impairment.To validate this hypothesis,we established rat models of chronic cerebral hypoperfusion（CCH） by the permanent occlusion of the common carotid arteries using the two-vessel occlusion method.Three weeks after modeling,rat models were intragastrically administered 0.1,0.2,and 0.4 mg/kg DSS,once a day,for 5 successive weeks.The Morris water maze test was performed to investigate CCH-induced learning and memory deficits.TUNEL assay was used to analyze apoptosis in the hippocampal CA1,CA3 regions and dentate gyrus.Hematoxylin-eosin staining was performed to observe the morphology of neurons in the hippocampal CA1,CA3 regions and dentate gyrus.Western blot analysis was performed to investigate the phosphorylation of PKA,ERK1/2 and CREB in the hippocampal PKA/ERK1/2/CREB signaling pathway.Results showed that DSS treatment greatly improved the learning and memory deficits of rats with CCH,reduced apoptosis of neurons in the hippocampal CA1,CA3 regions and dentate gyrus,and increased the phosphorylation of PKA,ERK1/2,and CREB in the hippocampus.These findings suggest that DSS protects against CCH-induced memory impairment and hippocampal damage possibly through activating the PKA/ERK1/2/CREB signaling pathway.展开更多
基金supported by the National Natural Science Foundation for Distinguished Young Scholars of China (30125014)
文摘Objective The existence of neuropsychological deficits has been implicated in obsessive-compulsive disorder （OCD）, particularly memory, attention, and executive functions. However, few studies have focused on neuropsychological deficits in the relatives of OCD patients. The aim of this study was to investigate cognitive deficits in OCD patients and their parents. Methods Forty patients with OCD, 48 parents of these patients, and 87 healthy controls completed a neuropsychological testing battery. Results Both OCD patients and their parents showed impairments in delayed verbal memory and delayed visual memory. Furthermore, they performed worse than healthy controls in problem-solving ability. Conclusion Our study demonstrated familial aggregation of delayed memory deficits and impaired problem-solving ability, which may be the potential neuropsychological endophenotypes of hereditary susceptibility to OCD.
文摘The purpose of this study was to determine if the substituted pyrimidine, CXB-909 (formerly known as KP544) which has been shown to amplify the effects of nerve growth factor in elevating choline-acetyltransferase activity in vitro, could attenuate memory deficits in the mu-p-75 saporin injected mouse model of Alzheimer’s disease (AD). Seventy-one, seven-week old C57/BL6 mice received daily oral intubation of 10, 15, or 20 mg/kg CXB-909, or vehicle (0.5% methylcellulose solution), which continued for 32 days. At postnatal week nine, mice received bilateral intra-cerebroventricular injections of mu-p-75 saporin, or sterile phosphate buffered saline. Seven days after surgery, mice were trained for two days, on a cued-platform version of the Morris water maze task, and then tested on a four-day hidden-platform version, followed by a one-day probe version of this task. Mice injected with mu-p-75 saporin, had increased latency to find the hidden-platform compared to sham mice. Furthermore, mice treated with CXB-909 at the 10, and 15 mg/kg doses, significantly reduced their latency to reach the hidden-platform, compared to vehicle-treated mice given mu-p-75 saporin. These results suggest that CXB-909 can attenuate memory deficits in the mu-p-75 saporin injected mouse model of AD.
文摘目的探讨正常老年大鼠空间学习记忆能力变化与海马背侧组织胆固醇代谢之间的关系。方法实验大鼠分老年实验组和青年对照组,利用Morris水迷宫方法评价空间学习记忆能力,然后测定海马背侧组织胆固醇含量及代谢相关酶羟甲基戊二酸单酰CoA还原酶(3-hydroxy-3-methylglutaryl coenzyme A reductase,HMG-CoAR)和胆固醇-24S-羟化酶(cholesterol24-hydroxylase,CYP46)mRNA表达的变化。结果与青年对照组相比,老年实验组逃避潜伏期明显延长(P<0.05),海马背侧组织总胆固醇的含量明显升高(P<0.05),HMG-CoAR mRNA相对表达量无明显变化,CYP46mRNA相对表达量明显降低(P<0.05)。结论正常老年大鼠空间学习记忆能力下降可能与海马背侧组织胆固醇含量增加有关。
文摘目的:观察中药健脑合剂对正常小鼠急性脑缺氧的保护作用及记忆障碍小鼠学习记忆的改善作用,并初步探讨其作用机理。方法:采用常压缺氧、亚硝酸钠缺氧及断头缺氧法观察健脑合剂对正常小鼠急性脑缺氧的保护作用;用跳台法、避暗法检测健脑合剂对由东莨菪碱、亚硝酸钠及乙醇所致记忆障碍小鼠的学习记忆能力的影响。结果:健脑合剂14g/kg 和28g/kg 对常压缺氧、亚酸钠缺氧及断头缺氧显示出显著延长急性脑缺氧状态下小鼠的生存时间的作用;同时显著增强小鼠被动学习能力,改善由东莨菪碱、亚硝酸钠及乙醇所致记忆获得、记忆巩固及记忆再现障碍。结论:中药健脑合剂对正常小鼠急性脑缺氧具有较好的保护作用并可改善记忆障碍模型小鼠学习记忆功能,其机制可能与提高大脑血氧水平、影响中枢 M 胆碱能系统等有关。
基金supported by the National Natural Science Foundation of China,No.81560583the Natural Science Foundation of Jiangxi Province of China,No.20142BAB205021
文摘3′-Daidzein sulfonate sodium（DSS） is a new synthetic water-soluble compound derived from daidzein,a soya isoflavone that plays regulatory roles in neurobiology.In this study,we hypothesized that the regulatory role of DSS in neurobiology exhibits therapeutic effects on hippocampal damage and memory impairment.To validate this hypothesis,we established rat models of chronic cerebral hypoperfusion（CCH） by the permanent occlusion of the common carotid arteries using the two-vessel occlusion method.Three weeks after modeling,rat models were intragastrically administered 0.1,0.2,and 0.4 mg/kg DSS,once a day,for 5 successive weeks.The Morris water maze test was performed to investigate CCH-induced learning and memory deficits.TUNEL assay was used to analyze apoptosis in the hippocampal CA1,CA3 regions and dentate gyrus.Hematoxylin-eosin staining was performed to observe the morphology of neurons in the hippocampal CA1,CA3 regions and dentate gyrus.Western blot analysis was performed to investigate the phosphorylation of PKA,ERK1/2 and CREB in the hippocampal PKA/ERK1/2/CREB signaling pathway.Results showed that DSS treatment greatly improved the learning and memory deficits of rats with CCH,reduced apoptosis of neurons in the hippocampal CA1,CA3 regions and dentate gyrus,and increased the phosphorylation of PKA,ERK1/2,and CREB in the hippocampus.These findings suggest that DSS protects against CCH-induced memory impairment and hippocampal damage possibly through activating the PKA/ERK1/2/CREB signaling pathway.
