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Amyotrophic Lateral Sclerosis (ALS), commonly known as Lou Gehrig's disease, is a progressive neurodegenerative disorder that leads to the death of neurons controlling voluntary muscles. Symptoms include muscle stiffness, twitching, and gradual weakness, ultimately causing the loss of critical functions like walking, speaking, and breathing. While most cases (90-95%) have no known cause and are likely influenced by genetic and environmental factors, around 5-10% are inherited.
At Naason Science, our Preclinical Research Models are instrumental in studying ALS pathology and evaluating potential treatments. These models replicate key aspects of ALS, such as motor neuron degeneration and muscle weakness, providing valuable insights into disease progression. By leveraging these models, we aim to advance the understanding of ALS and support the development of therapies that can improve patient outcomes and quality of life.
Riluzole is a medication that may slightly extend life expectancy by two to three months, but there is currently no cure for ALS. Some familial cases involve mutations in the copper/zinc superoxide dismutase (SOD-1) gene, and studies using G93A SOD-1 mice have provided insights into the disease's pathology, revealing a correlation between mutant SOD expression and motor neuron degeneration.
Species: Mice
Gene: Male/Female
Disease Relevance: Mutations in superoxide dismutase 1 gene (SOD1) with G93A mutation are linked to amyotrophic lateral sclerosis (ALS), a neurodegenerative disorder predominantly affecting upper and lower motor neurons. Robust muscle weakness can be observed.
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