The study investigates a transgenic rat model expressing the SOD1-G93A mutation, which mimics many of the key characteristics of Amyotrophic Lateral Sclerosis (ALS). These include motor neuron degeneration, progressive muscle dysfunction, and increased levels of the neurofilament light chain (NfL), a biomarker for neurodegeneration. The model is shown to be valuable for ALS drug development due to its ability to replicate crucial aspects of the disease, offering a reliable platform for testing potential therapies.
Explore this poster to learn about:
- The development of a rat model expressing human SOD1 with the G93A mutation and the significance of this mutation in ALS research.
- The examination of the ALS-like disease phenotypes observed in the SOD1-G93A rat model, including motor neuron degeneration and muscle dysfunction.
- Insights into how variability in the disease phenotype of the SOD1-G93A rat model is managed and incorporated into study design.
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