摘要
在脑神经元中保持适当的能量水平是由许多脑功能一起作用的结果,如突触传递,囊泡的回收和轴突的运输。AMP激活的蛋白激酶(AMPK)是所有活细胞的主要能量传感器。除此之外,其具有在下丘脑神经元重要的全身能量传感器的作用,AMPK也表示在整个大脑的神经元,它可能发挥其它的基础性作用。例如,AMPK可能参与了大脑的发育、神经元的极化和神经元的活动。此外,最近的证据表明,AMPK的反常可能参与神经退行性疾病如阿尔茨海默氏症,帕金森,亨廷顿病,肌萎缩侧索硬化及缺血性脑卒。因此,AMPK是这些神经退行性疾病新兴的潜在治疗靶点。在这里,我们将回顾最近的文献关于AMPK在脑的生理和病理作用并讨论其所产生的潜在治疗意义。
关键词: AMPK、阿尔茨海默病、帕金森病、Huntington病、肌萎缩性侧索硬化、缺血性中风、神经退行性疾病,神经发育。
图形摘要
Current Drug Targets
Title:AMPK in Neurodegenerative Diseases: Implications and Therapeutic Perspectives
Volume: 17 Issue: 8
Author(s): Claudia Marinangeli, Sébastien Didier, Valérie Vingtdeux
Affiliation:
关键词: AMPK、阿尔茨海默病、帕金森病、Huntington病、肌萎缩性侧索硬化、缺血性中风、神经退行性疾病,神经发育。
摘要: Maintaining proper energy levels in brain neurons is crucial for many cerebral functions such as synaptic transmission, vesicle recycling and axonal transport. AMP-activated protein kinase (AMPK) is the main energy sensor of all living cells. Beside its role as a crucial whole-body energy sensor in hypothalamic neurons, AMPK is also expressed in neurons throughout the brain where it might play additional fundamental roles. For instance, AMPK might be involved in brain development, neuronal polarization and neuronal activity. In addition, recent evidences suggest that AMPK deregulation might participate in neurodegenerative diseases such as Alzheimer’s, Parkinson’s, Huntington’s, amyotrophic lateral sclerosis and ischemic stroke. Therefore, AMPK is emerging as a potential therapeutic target for these neurodegenerative diseases. Here, we will review the recent literature regarding the physiological and pathological role of AMPK in the brain and discuss the resulting potential therapeutic implications.
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Cite this article as:
Claudia Marinangeli, Sébastien Didier, Valérie Vingtdeux , AMPK in Neurodegenerative Diseases: Implications and Therapeutic Perspectives, Current Drug Targets 2016; 17 (8) . https://dx.doi.org/10.2174/1389450117666160201105645
DOI https://dx.doi.org/10.2174/1389450117666160201105645 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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