Identification of dysphagia in a transgenic mouse model of amyotrophic lateral sclerosis

Abstract

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Previous work in our lab has established the SOD1-G93A transgenic mouse as a suitable model for dysphagia (swallowing impairment) in amyotrophic lateral sclerosis (ALS). This strain has significantly impaired lick and mastication rates at 8 weeks of age, which is the earliest time point tested to date. We have extended this previous work by testing mice post-weaning at 3, 5, and 7 weeks of age. At each time point, SOD1-G93A transgenic mice demonstrated a significantly slower lick rate compared with age-matched, nontransgenic controls (p<0.05). No group differences in mastication rate were identified. This early-onset impairment in lick rate suggests that SOD1-G93A transgenic mice may be a model of bulbar-onset rather than spinal-onset ALS. Therefore, the SOD1-G93A transgenic mouse may be uniquely suitable to studying the onset and progression of dysphagia in humans with bulbar-onset ALS, which occurs in [about]30% of cases.