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Duchenne Muscular Dystrophy (DMD) is a severe, progressive genetic disorder characterized by muscle degeneration and weakness due to mutations in the dystrophin gene. Primarily affecting young boys, DMD leads to symptoms such as difficulty walking, frequent falls, and muscle wasting, eventually impacting the heart and respiratory muscles. This condition significantly reduces quality of life and often limits life expectancy.
At Naason Science, our Preclinical Research Models for DMD are crucial for understanding the mechanisms of this disorder and assessing potential therapies. These models replicate the core aspects of DMD pathology, including dystrophin deficiency, muscle fiber damage, and functional impairment, allowing for a comprehensive evaluation of therapeutic strategies. Our models support the development of treatments aimed at slowing disease progression and improving the quality of life for individuals affected by DMD, bridging the gap from laboratory discoveries to clinical applications.
Duchenne Muscular Dystrophy (DMD) is a rare muscle-wasting disease caused by mutations in the dystrophin gene. Dystrophin provides structural support to muscle cell membranes during contraction and relaxation. When dystrophin is absent, muscles undergo degeneration, leading to muscle weakness and eventual heart and/or respiratory failure.
Understanding the disease phenotype in animal models is crucial for preclinical evaluations. DMD, an X-linked pediatric muscle disease caused by dystrophin gene mutations, results in the complete loss of dystrophin. Using mdx mice in research, while common, has limitations due to their milder phenotype compared to humans in modeling DMD treatments.
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