摘要
目的:血管性痴呆是主要由脑血管疾病引起的获得性、慢性、进行性认知障碍,是老年期痴呆的主要类型。其发病机制尚不明确。突触损伤可能是其早期的病理改变,与其认知功能障碍关系密切。资料来源:应用计算机检索Medline1990-01/2004-12关于血管性痴呆、脑缺血及认知障碍与突触改变的文章,检索词包括“cerebralis-chemiaandsynapse;cognitiveimpairmentandsynapse;vasculardemen-tiaandsynapse;demetianandsynapse,long-termprotection”等,并限定文章语言种类为English。应用计算机检索维普全文数据库1990-01/2004-12关于血管性痴呆、脑缺血及认知障碍与突触改变的文章,检索词为“突触结构,可塑性,血管性痴呆、突触功能,突触蛋白”。并限定语言种类为中文。资料选择:对资料进行初审,选择脑缺血时突触改变、认知障碍时突触改变、血管性痴呆时突触改变的文章,然后筛除与以上要求无明显联系的文章。排除重复性研究。资料提炼:共收集到78篇相关的中英文文献,排除43篇,纳入35篇,其中涉及血管性痴呆与突触13篇,脑缺血与突触17篇,认知障碍与突触22篇。资料综合:突触是神经元之间的结构和功能的接触点,突触的可塑性是学习记忆的神经生物学基础,血管性痴呆的发病过程中突触改变可能是其重要机制。突触形态结构的可塑性和传递效能的可塑性的物质基础都涉及神经元和突触部位的某些蛋白质、受体、神经递质、离子及信使分子的物理化学变化。目前研究较多的突触蛋白是突触膨体素、突触素、突触后致密结构-95等。结论:突触损伤在血管性痴呆发病的早期即存在,且与其认知功能障碍密切相关。对血管性痴呆发病中突触可塑性的研究有利于进一步阐明其发病机制,从而更有效地对其进行防治。
OBJECTIVE：Vascular dementia,which is the acquired,chronic and progressive cognitive impairments caused by cerebrovascular disease, is .the main type of senile dementia,and its pathogenesis is still not clear. Synaptic injury may be its early pathological changes,and it is closely correlated with cognitive dysfunction. DATA SOURCES：An overall retrieval for materials on vascular dementia, cerebral isehemia and cognitive impairment in correlation with synaptie changes published in English between January 1990 and December 2004 on Pubmed database was undertaken by using the keywords of ＂cerebral isehemia and synapse,cognitive impairment and synapse, vascular dementia and synapse,dementia and synapse,long-term protection＂.Meanwhile, Chinese articles about vascular dementia,cerebral ischemia,eognitive impairment and synaptie changes between January 1990 and December 2004 were searched in VIP full-text database, the keywords were ＂synaptie strueture, plastieity, vaseular dementia, synaptie funetion, synapsin＂in Chinese. STUDY SELECTION：The data were checked firstly,the articles about synaptie changes when cerebral ischemia,eognitive impairment and vascular dementia were collected, and then the obvious irrelative ones were screened out, and the repetitive studies were excluded. DATA EXTRACTION：Totally 78 relevant articles were collected,43 were deleted,and 35 accorded with the inclusive criteria, including 13 about vascular dementia and synapse,17 about cerebral isehemia and synapse, 22 about cognitive impairment and synapse. DATA SYNTHESIS：Synapse is the contact point of structure and .function between neurons,the synaptie plasticity is the neurobiologieal basis of study and memory.The synaptie changes may be the mechanism during the attack of vascular dementia.The material basis for the plasticities of synaptie morphological structure and convective function are all correlated with the physic and chemical changes of some protein, receptor, neurotransmitter, ion and messenger molecule in neurons and at synapse. CONCLUSlON：Synaptie injury exists at the early period of the attack of vascular dementia, and is closely;correlated with the cognitive dysfunction. Researches in synaptie plasticity during vascular dementia are contributive to the .clarification the pathogenesis of vascular dementia,which is advantageous to the prevention and cure of vascular dementia.
出处
《中国临床康复》
CSCD
北大核心
2005年第48期130-132,共3页
Chinese Journal of Clinical Rehabilitation
