Mattson Mark P, Gleichmann Marc, Cheng Aiwu
Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA.
Neuron. 2008 Dec 10;60(5):748-66. doi: 10.1016/j.neuron.2008.10.010.
Mitochondrial electron transport generates the ATP that is essential for the excitability and survival of neurons, and the protein phosphorylation reactions that mediate synaptic signaling and related long-term changes in neuronal structure and function. Mitochondria are highly dynamic organelles that divide, fuse, and move purposefully within axons and dendrites. Major functions of mitochondria in neurons include the regulation of Ca(2+) and redox signaling, developmental and synaptic plasticity, and the arbitration of cell survival and death. The importance of mitochondria in neurons is evident in the neurological phenotypes in rare diseases caused by mutations in mitochondrial genes. Mitochondria-mediated oxidative stress, perturbed Ca(2+) homeostasis, and apoptosis may also contribute to the pathogenesis of prominent neurological diseases including Alzheimer's, Parkinson's, and Huntington's diseases; stroke; amyotrophic lateral sclerosis; and psychiatric disorders. Advances in understanding the molecular and cell biology of mitochondria are leading to novel approaches for the prevention and treatment of neurological disorders.
线粒体电子传递产生的ATP对于神经元的兴奋性和存活至关重要，并且对于介导突触信号传导以及神经元结构和功能的相关长期变化的蛋白质磷酸化反应也必不可少。线粒体是高度动态的细胞器，可在轴突和树突内进行分裂、融合并定向移动。线粒体在神经元中的主要功能包括对Ca(2+)和氧化还原信号的调节、发育和突触可塑性以及细胞存活与死亡的调控。线粒体基因的突变导致的罕见疾病的神经学表型，证明了线粒体在神经元中的重要性。线粒体介导的氧化应激、Ca(2+)稳态紊乱和细胞凋亡也可能促成包括阿尔茨海默病、帕金森病和亨廷顿病在内的主要神经疾病、中风、肌萎缩侧索硬化症以及精神疾病的发病机制。对线粒体分子和细胞生物学认识的进展正带来预防和治疗神经疾病的新方法。
