The elucidation of the pathogenesis of dysphagia in amyotrophic lateral sclerosis -Using model mice-

ALS模型小鼠延髓腹侧舌下核神经元细胞死亡，背侧迷走神经背侧运动核神经元细胞未见死亡。发病后ALS模型小鼠的运动神经元受轴突损伤的程度较野生型小鼠和发病前小鼠更为严重。胶质瘤的程度反映了ALS（肌萎缩侧索硬化症）的病理进展。这些结果提示，Iba1（离子钙结合适配分子1）、Mac2（巨噬细胞特异性标记物2）和GFAP（胶质原纤维酸性蛋白）阳性胶质细胞的定位差异与ALS患者选择性运动神经元细胞死亡有关。

In the medulla oblongata of ALS model mice, neuronal cell death in neurons of the hypoglossal nucleus in the ventral part were observed, but the neuronal cell death was escaped in the neurons in the dorsal motor nucleus of the vagus nerve in the dorsal part. The motor neurons in the ALS model mice after the onset were more severely damaged by axonal injury than the motor neurons in the wild-type mice and pre-onset mice.The degree of gliosis reflected the progression of the pathology of ALS (amyotrophic lateral sclerosis). These results suggest that the difference in the localization of glial cells such as Iba1 (ionized calcium binding adapter molecule 1), Mac2 (macrophage specific marker 2) and GFAP (glial fibrillary acidic protein)-positive glial cell is associated with the selective motor neuronal cell death in ALS.