衰老动物和阿尔茨海默病动物模型中的突触可塑性损伤。
Impairments of synaptic plasticity in aged animals and in animal models of Alzheimer's disease.
机构信息
Neurobiology of Aging Laboratory, INRCA Scientific Technological Area, Ancona, Italy.
出版信息
Rejuvenation Res. 2012 Apr;15(2):235-8. doi: 10.1089/rej.2012.1318.
Abstract
Aging is associated with a gradual decline in cognitive functions, and more dramatic cognitive impairments occur in patients affected by Alzheimer's disease (AD). Electrophysiological and molecular studies performed in aged animals and in animal models of AD have shown that cognitive decline is associated with significant modifications in synaptic plasticity (i.e., activity-dependent changes in synaptic strength) and have elucidated some of the cellular mechanisms underlying this process. Morphological studies have revealed a correlation between the quality of memory performance and the extent of structural changes of synaptic contacts occurring during memory consolidation. We briefly review recent experimental evidence here.
摘要
衰老是认知功能逐渐下降的原因，而阿尔茨海默病（AD）患者的认知障碍更为明显。在老年动物和 AD 动物模型中进行的电生理和分子研究表明，认知能力下降与突触可塑性（即突触强度的活性依赖性变化）的显著改变有关，并阐明了这一过程背后的一些细胞机制。形态学研究揭示了记忆巩固过程中突触接触的结构变化程度与记忆表现质量之间的相关性。在这里，我们简要回顾了最近的实验证据。
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