Cognitive flexibility deficits in a mouse model for the absence of full-length dystrophin

摘要: Duchenne muscular dystrophy (DMD) is a progressive muscle-wasting disorder, caused by mutations in the DMD gene and resulting lack of dystrophin. The has seven promoters, giving rise to multiple full-length shorter isoforms. Besides expression dystrophin muscles, majority isoforms expressed brain dystrophinopathy can lead cognitive deficits, including intellectual impairments deficits executive function. In contrast muscle pathology, impact on not very well studied. Here, we study behavioral consequences mdx mice, particularly with regard domains functions anxiety. We observed deficit flexibility mice absence motor dysfunction or general learning using two independent tests. addition, increased anxiety was observed, but its depended context. Overall, these results suggest that specific effects compare patients.