Rygiel Karolina A, Grady John P, Turnbull Doug M
Newcastle University Centre for Brain Ageing and Vitality, Institute for Ageing and Health, The Medical School, Newcastle University, Newcastle upon Tyne, UK; Wellcome Trust Centre for Mitochondrial Research, Institute for Ageing and Health, The Medical School, Newcastle University, Newcastle upon Tyne, UK.
Wellcome Trust Centre for Mitochondrial Research, Institute for Ageing and Health, The Medical School, Newcastle University, Newcastle upon Tyne, UK.
Neurobiol Aging. 2014 Oct;35(10):2230-8. doi: 10.1016/j.neurobiolaging.2014.02.027. Epub 2014 Mar 3.
Sarcopenia, muscle wasting, and strength decline with age, is an important cause of loss of mobility in the elderly individuals. The underlying mechanisms are uncertain but likely to involve defects of motor nerve, neuromuscular junction, and muscle. Loss of motor neurons with age and subsequent denervation of skeletal muscle has been recognized as one of the contributing factors. This study investigated aspects of mitochondrial biology in spinal motor neurons from elderly subjects. We found that protein components of complex I of mitochondrial respiratory chain were reduced or absent in a proportion of aged motor neurons-a phenomenon not observed in fetal tissue. Further investigation showed that complex I-deficient cells had reduced mitochondrial DNA content and smaller soma size. We propose that mitochondrial dysfunction in these motor neurons could lead to the cell loss and ultimately denervation of muscle fibers.
肌肉减少症，即随着年龄增长出现的肌肉萎缩和力量下降，是老年人行动能力丧失的一个重要原因。其潜在机制尚不清楚，但可能涉及运动神经、神经肌肉接头和肌肉的缺陷。随着年龄增长运动神经元的丧失以及随后骨骼肌的去神经支配已被认为是促成因素之一。本研究调查了老年受试者脊髓运动神经元中线粒体生物学的相关方面。我们发现，在一部分老年运动神经元中，线粒体呼吸链复合体I的蛋白质成分减少或缺失——这一现象在胎儿组织中未观察到。进一步研究表明，复合体I缺陷的细胞线粒体DNA含量减少且胞体尺寸较小。我们认为，这些运动神经元中的线粒体功能障碍可能导致细胞丢失并最终使肌纤维去神经支配。
