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

• Project/Area Number: 23791921
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Otorhinolaryngology
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: SAITO Atsushi 京都府立医科大学, 医学(系)研究科(研究院), 助教 (80573633)
• Project Period (FY): 2011 – 2013
• Project Status: Completed (Fiscal Year 2013)
• Budget Amount: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000); Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000); Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000); Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
• Keywords: 嚥下障害 / ALS

Research Abstract

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.