So far as the defective variants of the SOD1 protein may interact with other cellular components to cause the disease remained unclear. Previous studies have shown, the transport process in slowing ALS patients and in related animal models read . However, it is unknown how the transport process is inhibited. The new results from the study by Zhu and his colleagues discovered a molecular mechanism for the defective transport in ALS. The results are described in the article Interaction between Familial Amyotrophic Lateral Sclerosis -linked SOD1 mutants and the dynein complex. .
The results of the study by Zhu and his colleagues indicate that the defective transport of molecules probably due to the interaction between the aberrant disease-causing mutants SOD1 and motor complex, intracellular transport intracellular transport in neurons. This provides new insights into ways to prevent or slow down ALS.
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