• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >CONTINUING THE SEARCH FOR CHOLINERGIC FACTORS IN COGNITIVE DYSFUNCTION
【24h】

CONTINUING THE SEARCH FOR CHOLINERGIC FACTORS IN COGNITIVE DYSFUNCTION

机译：在认知功能障碍中继续寻找胆碱能的因素

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The objective of the experiments reported here was to explore three hypotheses regarding cholinergic processes underlying the development of progressive degenerative dementia (PDD). One possibility involved the downregulation of muscarinic receptors (mAChR) with aging, thus reducing the capability of the cholinergic system to support normal memory and other cognitive functions. The results of downregulation to 10% of normal produced only a temporary effect, the system having the capability to repair the damage. A second hypothesis predicted that a chronic hypocholinergic state can produce structural changes that are reflected in persisting cognitive dysfunctions. Chronic administration of a false cholinergic transmitter in the diets of weanling rats mimicked such a state which, if maintained for a protracted period, produced many of the features of PDD in humans. When the diet was returned to normal, biochemical and physiological processes recovered fully. However, memory impairment continued. This suggested the possibility that the behavioral losses were mediated by persisting morphological changes in the CNS. The third hypothesis proposes that these changes may be due to cell loss resulting from impaired phospholipid metabolism. Changes in sphingomyelin, one of the two major Ch-containing lipids in cell membranes, could increase amounts of ceramide, an inducer of programmed cell death (apoptosis). Tests of this hypothesis are nearing completion. [References: 15]
机译：本文报道的实验的目的是探索关于进行性退行性痴呆（PDD）发展的胆碱能过程的三个假设。一种可能性涉及随着年龄的增长而下调毒蕈碱受体（mAChR），从而降低胆碱能系统支持正常记忆和其他认知功能的能力。下调至正常水平的10％的结果仅产生暂时效果，该系统具有修复损伤的能力。第二种假设预测，慢性低胆碱能状态可以产生结构性变化，反映在持续的认知功能障碍中。在断奶大鼠的饮食中长期施用假胆碱能递质可模仿这种状态，如果长期维持，会在人体内产生许多PDD功能。当饮食恢复正常后，生化和生理过程完全恢复。但是，记忆障碍继续。这表明行为丧失可能是由中枢神经系统持续的形态变化所介导的。第三个假设提出，这些变化可能是由于磷脂代谢受损导致的细胞丢失所致。鞘磷脂是细胞膜中两种主要的含Ch脂质之一，其变化可能增加神经酰胺的含量，神经酰胺是程序性细胞死亡（细胞凋亡）的诱导剂。该假设的检验即将完成。 [参考：15]

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号