Increased preservation of muscle strength is observed in the mdx3cv mouse due to expression of near full-length dystrophin at ~5% of normal levels.64 Unlike the other mdxcv variants, the mdx3cv mutation affects isoforms of dystrophin in other tissues, and has been shown to exhibit non-muscle phenotypes such as cognitive defects,65 abnormal electroretinogram66 and low reproductive rate.67 The mdx4cv and mdx5cv models have a nonsense mutation resulting in a premature stop codon in exon 53, and a point mutation resulting in a new splice site in exon 10, respectively. The gene discussed is DMD; the disease is Cognitive impairment.