AMYOTROPHIC-LATERAL-SCLEROSIS - LOWER MOTOR-NEURON DISEASE SPREADING TO UPPER MOTOR-NEURONS
AMYOTROPHIC-LATERAL-SCLEROSIS - LOWER MOTOR-NEURON DISEASE SPREADING TO UPPER MOTOR-NEURONS
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DOI：
10.1002/mus.880160810
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发表时间：
1993-08-01
期刊：
影响因子：
3.4
通讯作者：
NORRIS, FH
中科院分区：
文献类型：
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作者：
CHOU, SM;NORRIS, FH
与最近重新强调的肌萎缩侧索硬化症（ALS）中涉及的主要神经元是皮质（上）运动神经元（UMN）的观点相反，我们认为下运动神经元（LMN）主要参与神经肌肉接头病原体的逆行运输，疾病过程单突触扩散到UMN。病理学和流行病学，LMN假说是更合乎逻辑的比UMN在最近的理解神经轴突运输系统，特别是在顺行细胞骨架运输和动力学的力量，促进缓慢轴突运输。通过关联早期病理学发现，即，LMN中原始轴突肿胀和胞浆内包涵体形成，ALS可被认为是轴突运输疾病，尤其是其慢成分（SCa）。应尝试在ALS中进行治疗干预以促进SCa。
Contrary to the recently reemphasized notion that the primary neuron involved in amyotrophic lateral sclerosis (ALS) is the cortical (upper) motor neuron (UMN), we believe that the lower motor neuron (LMN) is primarily involved by the retrograde transport of pathogens from neuromuscular junctions, and the disease process spreads monosynaptically to the UMN. Pathologically and epidemiologically, the LMN hypothesis is more logical than the UMN in light of the recent understanding of neuroaxonal transport systems, particularly in regard to anterograde cytoskeleton transport and the kinetics of the force promoting slow axonal transport. By correlating the early pathologic findings, i.e., the swelling of the initial axons and formation of intracytoplasmic inclusions in the LMN, ALS may be regarded as a disease of axonal transport, especially its slow component (SCa). Therapeutic intervention to facilitate SCa should be attempted in ALS.