Tretter Brittany L, Dolbow David R, Ooi Vincent, Farkas Gary J, Miller Joshua M, Deitrich Jakob N, Gorgey Ashraf S
College of Osteopathic Medicine, William Carey University, Hattiesburg, MS 39401, USA.
Physical Therapy Program, William Carey University, Hattiesburg, MS 39401, USA.
J Clin Med. 2024 Nov 27;13(23):7197. doi: 10.3390/jcm13237197.
Emanating from several decades of study into the effects of the aging process after spinal cord injury (SCI), "accelerated aging" has become a common expression as the SCI accelerates the onset of age-related pathologies. However, the aging process follows a distinct trajectory, characterized by unique patterns of decline that differ from those observed in the general population without SCI. Aging brings significant changes to muscles, bones, and hormones, impacting overall physical function. Muscle mass and strength begin to decrease with a reduction in muscle fibers and impaired repair mechanisms. Bones become susceptible to fractures as bone density decreases. Hormonal changes combined with decreased physical activity accelerate the reduction of muscle mass and increase in body fat. Muscle atrophy and skeletal muscle fiber type transformation occur rapidly and in a unique pattern after SCI. Bone loss develops more rapidly and results in an increased risk of fractures in body regions unique to individuals with SCI. Other factors, such as excessive adiposity, decreased testosterone and human growth hormone, and increased systemic inflammation, contribute to a higher risk of neuropathically driven obesity, dyslipidemia, glucose intolerance, insulin resistance, and increasing cardiovascular disease risk. Cardiorespiratory changes after SCI result in lower exercise heart rates, decreased oxygenation, and mitochondrial dysfunction. While it is important to acknowledge the accelerated aging processes after SCI, it is essential to recognize the distinct differences in the aging process between individuals without physical disabilities and those with SCI. These differences, influenced by neuropathology, indicate that it may be more accurate to describe the aging process in individuals with chronic SCI as neurogenic accelerated aging (NAA). Research should continue to address conditions associated with NAA and how to ameliorate the accelerated rate of premature age-related conditions. This review focuses on the NAA processes and the differences between them and the aging process in those without SCI. Recommendations are provided to help slow the development of premature aging conditions.
经过数十年对脊髓损伤(SCI)后衰老过程影响的研究,“加速衰老”已成为一个常用表述,因为脊髓损伤会加速与年龄相关的病理状况的出现。然而,衰老过程遵循着一条独特的轨迹,其特征是独特的衰退模式,与未患脊髓损伤的普通人群中观察到的模式不同。衰老给肌肉、骨骼和激素带来显著变化,影响整体身体功能。肌肉质量和力量开始下降,肌肉纤维减少且修复机制受损。随着骨密度降低,骨骼变得易骨折。激素变化与身体活动减少相结合,加速了肌肉质量的减少和体脂增加。脊髓损伤后,肌肉萎缩和骨骼肌纤维类型转变迅速且以独特模式发生。骨质流失发展更快,导致脊髓损伤患者身体特定部位骨折风险增加。其他因素,如过度肥胖、睾酮和人类生长激素减少以及全身炎症增加,会导致神经病理性肥胖、血脂异常、葡萄糖不耐受、胰岛素抵抗风险升高,以及心血管疾病风险增加。脊髓损伤后的心肺变化导致运动心率降低、氧合减少和线粒体功能障碍。虽然认识到脊髓损伤后的加速衰老过程很重要,但必须认识到无身体残疾者与脊髓损伤者衰老过程的明显差异。这些受神经病理学影响的差异表明,将慢性脊髓损伤患者的衰老过程描述为神经源性加速衰老(NAA)可能更准确。研究应继续关注与神经源性加速衰老相关的状况以及如何改善过早出现的与年龄相关状况的加速速度。本综述重点关注神经源性加速衰老过程以及它们与未患脊髓损伤者衰老过程的差异。还提供了有助于减缓过早衰老状况发展的建议。