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

阐明肌萎缩侧索硬化症吞咽困难的发病机制 -使用模型小鼠 -

• 批准号: 23791921
• 负责人: SAITO Atsushi
• 金额: $ 2.16万
• 依托单位: Kyoto Prefectural University of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23791921/
• 关键词: 嚥下障害; ALS

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.

ALS模型小鼠延髓腹侧舌下核神经元有神经元死亡，而迷走神经背侧运动核神经元无神经元死亡。ALS模型小鼠发病后运动神经元受到轴突损伤的程度比野生型小鼠和发病前小鼠更严重，胶质细胞增生的程度反映了ALS(肌萎缩侧索硬化症)的病理进展。提示Iba1、Mac2、GFAP等神经胶质细胞的定位差异与ALS运动神经细胞的选择性死亡有关。