Calcium signaling and molecular mechanisms underlying neurodegenerative diseases.

Calcium signaling and molecular mechanisms underlying neurodegenerative diseases.
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DOI:
10.1016/j.ceca.2017.06.008
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发表时间:
2018-03
期刊:
影响因子:
4
通讯作者:
Bezprozvanny I
Bezprozvanny I
中科院分区:
生物学2区
文献类型:
--
作者:
Pchitskaya E;Popugaeva E;Bezprozvanny I

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钙离子(Ca2+)是真核细胞中普遍存在的第二信使,调节着细胞的各种活动。钙在可兴奋细胞中起着特别重要的作用。神经元需要对钙依赖性过程进行极其精确的时空控制,因为它们调节突触可塑性等重要功能。近年来的研究表明,在阿尔茨海默病(Alzheimer's disease,AD)、亨廷顿病(Huntington's disease,HD)和帕金森病(Parkinson's disease,PD)等神经退行性疾病中,神经元钙信号异常。这些疾病是一个重大的医疗、社会、财政和科学问题,但尽管作出了巨大的研究努力,它们仍然无法治愈,只能得到对症的缓解药物。因此,需要新的方法和目标。本文综述了神经元钙信号异常在这些疾病中的作用,特别强调了神经元钙库操纵的钙内流(SOCE)通路的作用及其作为神经退行性疾病治疗靶点的潜在意义。
Calcium (Ca2+) is a ubiquitous second messenger that regulates various activities in eukaryotic cells. Especially important role calcium plays in excitable cells. Neurons require extremely precise spatial-temporal control of calcium-dependent processes because they regulate such vital functions as synaptic plasticity. Recent evidence indicates that neuronal calcium signaling is abnormal in many of neurodegenerative disorders such as Alzheimer’s disease (AD), Huntington’s disease (HD) and Parkinson’s disease (PD). These diseases represent a major medical, social, financial and scientific problem, but despite enormous research efforts, they are still incurable and only symptomatic relief drugs are available. Thus, new approaches and targets are needed. This review highlight neuronal calcium-signaling abnormalities in these diseases, with particular emphasis on the role of neuronal store-operated Ca2+ entry (SOCE) pathway and its potential relevance as a therapeutic target for treatment of neurodegeneration.
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