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1.
背景以往研究表明精神分裂症患者的神经认知缺损和精神病性症状会导致其职业和社会功能降低。目的评估中国精神分裂症男性住院患者的神经认知和精神病性症状与社会心理功能之间的关系。方法选取上海市精神卫生中心的51例住院男性精神分裂症患者,其中40例患者最终完成了个体和社会功能量表(Personal and Social Performance Scale,PSP)中文版、临床疗效总评量表-病情严重程度量表(Clinical Global Impression-Severity,CGI-S)、阳性和阴性症状量表(Positive and Negative Symptom Scale,PANSS)、字母-数字排序以及香港文字记忆学习测试等项目的评定。结果患者PANSS量表的3个临床分量表的分值和社会功能总体评估(PSP总分和CGI-S分值)之间存在明显负相关。患者的神经认知测定结果与症状或社会功能状况均无关。结论对于急性期住院精神分裂症患者而言,临床症状的严重度—而非神经认知缺损程度,与其社会功能水平密切相关。  相似文献   

2.
目的探讨精神分裂症恢复期患者认知功能对社会功能的影响。方法对80例精神分裂症恢复期患者采用瑞文标准测验(CRT)、韦氏成人智力量表(WAIS)、威斯康星卡片测验(WCST),分别与社会功能缺陷量表(SDSS)进行多重线性回归分析。结果经逐步回归分析显示,WCST中变量(正确反应数、持续错误数、分类数)、WAIS中言语量表分、CRT中瑞文总分进入回归方程,拟合的回归方程均有统计学意义。其中瑞文总分、言语量表分与SDSS呈线性负相关关系,持续错误数与SDSS呈线性正相关关系;比较WCST、CRT、WAIS与SDSS的相关性,回归模型的拟合最好的为WCST。结论精神分裂症患者的认知功能与社会功能有显著相关性,正确的评测及改善认知功能对提高患者的社会功能有重要意义,WCST提供了一个有效预测精神分裂症患者社会功能的重要方法。  相似文献   

3.
为进一步了解精神分裂症神经生物学机制并为未来的相关研究及诊疗提供新思路,故对精神分裂症认知功能损伤的研究进行综述。认知功能受损是精神分裂症的重要临床表现之一。目前使用蒙特利尔认知评估量表(MoCA)及精神分裂症认知功能成套测验共识版(MCCB)评定精神分裂症患者的认知功能均发现患者存在严重的工作记忆障碍。工作记忆是大脑前额叶皮质的主要功能之一,而纹状体突触前合成和分泌的多巴胺(DA)含量与认知功能损伤程度及前额叶皮质功能存在相关性。对认知功能损伤的治疗有助于改善精神分裂症患者的预后、减轻社会负担。目前已有多种治疗方式可供选择。  相似文献   

4.
目的了解奥氮平和氯氮平对慢性精神分裂症患者的认知功能的影响。方法78例经典型抗精神病药物治疗疗效不显著或不能耐受不良反应的慢性精神分裂症患者随机替换为奥氮平及氯氮平治疗,分别在入组前、12周、6个月进行PANSS量表评定、认知功能测定,包括言语学习、记忆、注意、执行功能、精神运动。结果奥氮平组32例和氯氮平组34例完成了6个月的治疗,这些患者疗程结束时均显示精神症状显著改善,认知功能显著提高,表现为言语流畅性、言语学习、言语视觉记忆、执行功能方面。二者之间无显著差异。结论奥氮平和氯氮平均可改善慢性精神分裂症的认知功能,且二者的疗效相似。  相似文献   

5.
奥氮平对首发精神分裂症患者的疗效及认知功能影响   总被引:1,自引:0,他引:1  
目的观察奥氮平对首发精神分裂症患者的疗效及认知功能的影响。方法对31例首发精神分裂症患者在奥氮平治疗前及治疗12周后,用阳性症状量表(SAPS)、阴性症状量表(SANS)、韦氏成人智力量表(WAIS—R)、韦氏记忆量表(WMS)、简明精神病评定量表(BPRS)、韦斯康星卡片分类测验(WCST)进行评估,并观察奥氮平对精神分裂症症状的疗效及对认知功能的影响。结果治疗后SAPS、SANS、BPRS〈WCST中错误应答数的评估分值显著降低(P〈0.01),且非持续性错误、WMS的再生、理解评估分值也明显降低(P〈0.05)。结论奥氮平治疗精神分裂症疗效可靠并可显著改善部分患者的认知功能。  相似文献   

6.
长期住院对精神分裂症患者认知功能的影响   总被引:1,自引:0,他引:1  
目的:探讨长期住院对精神分裂症患者认知功能的影响。方法:对56例长期住院(≥5年)与49例住院时间较短(≤1年)的精神分裂症患者的精神症状和认知功能进行比较,采用阳性与阴性症状量表(PANSS)、韦氏成人智力量表(WAIS-R)、威斯康星卡片分类试验(WCST)等评定患者的认知功能。结果:长期住院(≥5年)组在智商、注意、记忆,以及信息整合与执行功能等均显著较差。结论:长期住院对精神分裂症患者认知功能有负面影响。  相似文献   

7.
本文目的是综述精神分裂症患者肠道菌群失调对认知功能受损的影响,为改善精神分裂症患者认知功能受损情况的新方法提供参考。精神分裂症患者的认知功能受损普遍存在,是阻碍其重返社会的重要原因之一。随着肠道菌群-肠-脑轴概念的提出,许多研究者发现精神分裂症患者肠道菌群失调与认知功能受损存在一定联系,本文阐述并总结既往研究中发现的此种联系,以期为改善精神分裂症患者认知功能受损情况提供参考。  相似文献   

8.
文拉法辛治疗精神分裂症患者认知功能障碍的疗效   总被引:1,自引:0,他引:1  
目的:探讨文拉法辛对精神分裂症患者认知功能障碍的治疗作用。方法:对43例达到显著进步以上的精神分裂症患者,随机分为文拉法辛组(22例)和对照组(2l例)分别给予文拉法辛和安慰剂治疗6周。采用韦氏成人智力量表(WAIS)、韦氏记忆量表(WMS)、威斯康星卡片分类测验(WCST)及副反应量表(TESS)进行评分。结果:治疗后以文拉法辛组认知功能改善显著较好。结论:文拉法辛对改善精神分裂症患者的认知功能障碍有益。  相似文献   

9.
双益平对精神分裂症患者认知功能影响的对照研究   总被引:2,自引:0,他引:2  
目的观察双益平对精神分裂症患者认知功能的影响。方法将76例诊断为精神分裂症的患者随机分成2组,其中一组(n=36)给予双益平治疗;另一组(n=40)为对照组,治疗8周,在入组前、治疗8周末分别进行韦氏成人智力量表(WAIS-RC)、韦氏记忆量表(WMS)、威斯康星卡片分类测验(WCST)及副反应量表(TESS)评分,比较双益平组对精神分裂症患者认知功能产生的影响。结果两组8周后,双益平组认知功能的改善与对照组比较差异有显著性。结论双益平能改善精神分裂症患者的认知功能,其中尤以对记忆的改善为突出。  相似文献   

10.
利培酮维持治疗精神分裂症3年疗效观察   总被引:5,自引:0,他引:5  
目的探讨利培酮治疗精神分裂症的长期疗效、安全性及其对认知功能的影响。方法92 例利培酮治疗的精神分裂症患者完成为期3年的观察,采用了阴性和阳性症状量表(PANSS)、简明精神病评定量表(BPRS)、副反应量表(TESS)、简易精神状态检查量表(MMSE)评定药物治疗的疗效与安全性及其对认知功能的影响。结果利培酮维持治疗期间,BPRS持续下降,疗效好,副作用少,不影响患者认知功能。结论利培酮治疗精神分裂症远期疗效稳定,安全性高,有利于患者重返社会。  相似文献   

11.
Late-onset Alzheimer's disease (LOAD) is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.  相似文献   

12.
Alzheimer's disease (AD) is the most common type of dementia, comprising an estimated 60-80% of all dementia cases. It is clinically characterized by impairments of memory and other cognitive functions. Previous studies have demonstrated that these impairments are associated with abnormal structural and functional connections among brain regions, leading to a disconnection concept of AD. With the advent of a combination of non-invasive neuroimaging (structural magnetic resonance imaging (MRI), diffusion MRI, and functional MRI) and neurophysiological techniques (electroencephalography and magnetoencephaJography) with graph theoretical analysis, recent studies have shown that patients with AD and mild cognitive impairment (MCI), the prodromal stage of AD, exhibit disrupted topological organization in large-scale brain networks (i.e., connectomics) and that this disruption is significantly correlated with the decline of cognitive functions. In this review, we summarize the recent progress of brain connectomics in AD and MCI, focusing on the changes in the topological organization of large-scale structural and functional brain networks using graph theoretical approaches. Based on the two different perspectives of information segregation and integration, the literature reviewed here suggests that AD and MCI are associated with disrupted segregation and integration in brain networks. Thus, these connectomics studies open up a new window for understanding the pathophysiological mechanisms of AD and demonstrate the potential to uncover imaging biomarkers for clinical diagnosis and treatment evaluation for this disease.  相似文献   

13.
There are several major pathological changes in Alzheimer's disease, including apoptosis of cho- linergic neurons, overactivity or overexpression of 13-site amyloid precursor protein cleaving enzyme 1 (BACE1) and inflammation. In this study, we synthesized a 19-nt oligonucleotide targeting BACE1, the key enzyme in amyloid beta protein (AI3) production, and introduced it into the pSilenCircle vector to construct a short hairpin (shRNA) expression plasmid against the BACE1 gene. We transfected this vector into C17.2 neural stem cells and primary neural stem cells, resulting in downregulation of the BACE1 gene, which in turn induced a considerable reduction in reducing AI3 protein production. We anticipate that this technique combining cell transplantation and gene ther- apy will open up novel therapeutic avenues for Alzheimer's disease, particularly because it can be used to simultaneously target several pathogenetic changes in the disease.  相似文献   

14.
阿尔茨海默病(AD)是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5~10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。  相似文献   

15.
BACKGROUND: Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes (safe time limit). Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE: To investigate the effects of transient cerebral ischemia (5 minutes)/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 (AQP-4) expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS: Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS: A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups: sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES: The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS: There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group (P 〉 0.05). However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group (P 〈 0.05 or P 〈 0.01). Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased (P 〈 0.05 or P 〈 0.01 ). Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days (P 〈 0.01). CONCLUSION: Transient cerebral ischemia (5 minutes) resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.  相似文献   

16.
BACKGROUND: Total saponins of Panax ginseng (TSPG) exhibits neuroprotection against Parkinson's disease in the substantia nigra. OBJECTIVE: To investigate the effects of TSPG on human embryonic neural stem cells (NSCs) proliferation and differentiation into dopaminergic neurons using in vitro studies, and to observe NSC differentiation in a mouse model of Parkinson's disease, as well as behavioral changes before and after transplantation. DESIGN, TIME AND SETTING: In vitro neural cell biology trial and in vivo randomized, controlled animal trial were performed at the Institute of Basic Medical Sciences, Chongqing Medical University between September 2004 and December 2007. MATERIALS: TSPG (purity 〉 95%) was isolated, extracted, and identified by Chongqing Academy of Chinese Materia Medica. Recombinant human basic fibroblast growth factor (bFGF) and recombinant human epidermal growth factor (EGF) were purchased from PeproTech, USA. A total of 25 C57/BL6J mice, aged 18-20 weeks were included. Twenty were used to establish a Parkinson's disease model with i.p. injection of MPTP (1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine) and TSPG alone or combined with interleukin-1 (IL-1)-treated NSCs prior to transplantation into the corpus striatum. The remaining five mice were pretreated for 3 days with TSPG prior to MPTP injection, serving as the TSPG prevention group. METHODS: Primary NSCs were isolated, cultured and purified from embryonic cerebral cortex. Immunocytochemistry was employed to detect specific antigen expression in the NSCs. In vitro experiment: (1) to induce proliferation, NSCs were treated with TSPG, EGF+bFGF, or TSPG+EGF+bFGF, respectively; (2) to induce dopaminergic neuronal differentiation, NSCs were treated with TSPG, IL-1, or TSPG+IL-1, respectively. MAIN OUTCOME MEASURES: In vitro experiment: the effects of TSPG on NSCs proliferation were evaluated with flow cytometry and MTT assay. Tyrosine hydroxylase expression was determined by immunocytochemistry assay to observe effects of TSPG on dopaminergic neuronal differentiation. In vivo experiment: differentiation of grafted NSCs in the mouse brain was determined by immunohistochemical staining. Behavioral changes were evaluated by spontaneous activity frequency, memory function, and score of paralysis agitans. RESULTS: (1) NSCs were cultured and passaged for more than three passages. Immunocytochemistry revealed positive nestin staining, as well as neurofilament protein and glial fibrillary acidic protein. (2) TSPG significantly increased NSC proliferation, in particular when combined with EGF and bFGF, which was twice as effective as FGF or bFGF alone. TSPG also induced dopaminergic differentiation in NSCs, in particular when TSPG was added together with IL-1, resulting in an effect five times greater than that of IL-1 alone. (3) At day 30 following transplantation, most NSCs in the TSPG prevention group differentiated into dopaminergic neurons, and the scores of paralysis agitans, spontaneous activity, and memory function were significantly increased compared with TSPG alone or TSPG+IL-1 groups (P 〈 0.05). CONCLUSION: TSPG stimulated NSC proliferation, in particular when combined with FGF and bFGF. TSPG significantly induced dopaminergic neuronal differentiation of NSCs, and the effect was greater when combined with IL-1. In addition, TSPG greatly improved behavior in the Parkinson's disease mouse model following NSC transplantation. Following NSC transplantation, TSPG pretreatment exhibited superior efficacy over either TSPG alone or TSPG in combination with IL-1, in terms of behavioral improvements in the Parkinson's disease mouse model.  相似文献   

17.
墨蝶呤还原酶(SPR)催化四氢生物蝶呤(BH4)从头合成途径的最后一步反应。SPR基因遗传缺陷或突变可导致BH。的合成紊乱,影响单胺类神经递质(如多巴胺、5-羟色胺及谷氨酸等)的合成或释放,进而参与包括精神分裂症在内的多种神经精神系统疾病的发生发展过程。此外,SPR基因敲除小鼠表现出持续增强的自主活动等类精神分裂症症状,说明该基因在精神分裂症的发病中扮演重要的角色。进一步研究SPR基因及其单核苷酸多态性的功能,可为阐明精神分裂症的发病机制提供重要的线索,也为新一代抗精神病药物的研制及开发开拓新的视野。现对SPR基因与精神分裂症的相关研究做一综述。  相似文献   

18.
目的通过检测癫痫大鼠海马神经元P13K、Akt和mTOR蛋白表达,探讨雷公藤内酯抑制癫痫大鼠神经元凋亡的分子机制。方法30只大鼠随机分为对照组、海人酸组、雷公藤内酯干预组,免疫组化法检测各组大鼠海马神经元P13K、Akt和mTOR蛋白的表达情况。结果海人酸组神经元胞体皱缩,形态不规则,数量减少,而雷公藤内酯干预组神经元的数量和形态与对照组相似,海人酸组海马神经元P13K、Akt、ITITOR蛋白表达与对照组比较均减少,而雷公藤内酯干预组海马神经元的P13K、Akt、mTOR蛋白表达均较海人酸组增加,差异均有统计学意义(P〈0.05)。结论雷公藤内酯可能通过上调P13K/Akt/mTOR信号通路蛋白表达对癫痫大鼠海马神经元发挥保护作用。  相似文献   

19.
20.
Neuronal autophagy is essential for neuronal survival and the maintenance of neuronal homeostasis. Increasing evidence has implicated autophagic dysfunction in the pathogenesis of Alzheimer's disease (AD). The mechanisms underlying autophagic failure in AD involve several steps, from autophagosome formation to degradation. The effect of modulating autophagy is context-dependent. Stimulation of autophagy is not always beneficial. During the implementation of therapies that modulate autophagy, the nature of the autophagic defect, the timing of intervention, and the optimal level and duration of modulation should be fully considered.  相似文献   

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