Duchenne muscular dystrophy (DMD) is an X-linked recessive genetic disorder, marked by progressive muscle degeneration due to the absence or impairment of the dystrophin protein. Our laboratory has been developing methods for gene therapy of DMD. The dystrophin gene is the largest known gene, which complicates gene therapy. We have shown that gene delivery vectors based on adeno-associated virus (AAV) can be used to deliver new genes body wide. However, AAV has a ~5 kb carrying capacity, so we have been developing miniaturized dystrophins. These smaller, highly functional dystrophins, which we named micro-dystrophin (µdys) were tested in a transgenic mdx4cv mouse model for DMD. Furthermore, we sought to develop a non-invasive method to evaluate treatment efficiency of µdys. In this project, the gait of mdx4cv, wild type (WT) and transgenic mice were observed to deduce potential benefits of the µdys transgene. We hypothesized that µdys treatment will enable the gait of the transgenic mice to resemble that of WT animals as opposed to mdx4cv. To test this, gait was assessed at three time points: 1.5, 3 and 6 months of age using the video-based Noldus CatWalk XT. Our results show that the length of a single stride of the transgenic mice hind paws increased over time compared to mdx4cv. The normal walking pattern of mice consists of placing diagonal paws on the surface, one front and one hind from opposite sides. In the case of mdx4cv, more paws were placed down for majority of the walk, as a compensatory mechanism for muscle weakness. The transgenic mice were found to walk with a diagonal pattern more frequently, like WT mice. Similarities in the gait of transgenic and WT mice help us conclude the µdys treatment was successfully able to mitigate the effects of DMD as seen by the gait analysis.