Sasaki Yo
Department of Genetics, Washington University in St. Louis, Couch Biomedical Research Building, 4515 McKinley Ave., Saint Louis, MO, 63110, United States.
Neurosci Res. 2019 Feb;139:9-20. doi: 10.1016/j.neures.2018.07.001. Epub 2018 Jul 10.
Cellular metabolism maintains the life of cells, allowing energy production required for building cellular constituents and maintaining homeostasis under constantly changing external environments. Neuronal cells maintain their structure and function for the entire life of organisms and the loss of neurons, with limited neurogenesis in adults, directly causes loss of complexity in the neuronal networks. The nervous system organizes the neurons by placing cell bodies containing nuclei of similar types of neurons in discrete regions. Accordingly, axons must travel great distances to connect different types of neurons and peripheral organs. The enormous surface area of neurons makes them high-energy demanding to keep their membrane potential. Distal axon survival is dependent on axonal transport that is another energy demanding process. All of these factors make metabolic stress a potential risk factor for neuronal death and neuronal degeneration often associated with metabolic diseases. This review discusses recent findings on metabolic dysregulations under neuronal degeneration and pathways protecting neurons in these conditions.
细胞代谢维持细胞的生命，使细胞能够产生能量，用于构建细胞成分，并在不断变化的外部环境中维持体内平衡。神经元细胞在生物体的整个生命周期中维持其结构和功能，并且由于成体中神经发生有限，神经元的丧失会直接导致神经网络复杂性的丧失。神经系统通过将含有相似类型神经元细胞核的细胞体放置在离散区域来组织神经元。因此，轴突必须长距离传输以连接不同类型的神经元和外周器官。神经元巨大的表面积使其需要大量能量来维持其膜电位。轴突远端的存活依赖于轴突运输，而这也是一个需要能量的过程。所有这些因素使得代谢应激成为神经元死亡的潜在风险因素，并且神经元变性通常与代谢疾病相关。本综述讨论了神经元变性时代谢失调的最新研究结果以及在这些情况下保护神经元的途径。
