Xiang Qiong, Li Xian-Hui, Fang Xin-Xing, Jia Jing, Ren Jie, Dong Yu-Chun, Ou-Yang Cheng
Technol Health Care. 2018;26(2):271-278. doi: 10.3233/THC-170978.
The aging-related disease and associated neurodegenerative complications, such as cognitive impairment, has received increasing attention.
The aim of this study was to show changes in cognitive behavior and molecular related the synaptic plasticity in aged-induced cognitive deficits rats.
We used novel object recognition testing and morphological staining as well as western blot to detect changes in cognitive behavior and molecular related the synaptic plasticity.
The morphological changes of synaptic structure and number on hippocampal neurons and learning and memory deficits were shown during natural aging. Moreover, learning and memory improvement was associated with alterations of hippocampal synaptic plasticity-related proteins, such as SNAP-25, synaptophysin, snapsoin-1 and so on, which distributes to cognitive decline in natural aging.
Our study provides more behavior and molecular evidence on relationship of cognitive deficits and aging.
与衰老相关的疾病以及相关的神经退行性并发症,如认知障碍,已受到越来越多的关注。
本研究旨在展示衰老诱导的认知缺陷大鼠认知行为的变化以及与突触可塑性相关的分子变化。
我们采用新物体识别测试、形态学染色以及蛋白质免疫印迹法来检测认知行为的变化以及与突触可塑性相关的分子变化。
在自然衰老过程中,海马神经元的突触结构和数量出现形态学变化,同时出现学习和记忆缺陷。此外,学习和记忆的改善与海马突触可塑性相关蛋白的改变有关,如突触小体相关蛋白25(SNAP-25)、突触素、小突触泡蛋白-1等,这些变化导致自然衰老过程中的认知衰退。
我们的研究为认知缺陷与衰老之间的关系提供了更多行为学和分子学证据。