ansport in several diseases, including SBMA, in which a mutation in the receptor for testosterone leads to the loss of motor neurons. In the new study, Brady and his co-workers were able to show that polyQ-AR, the mutated protein in SBMA, caused inhibition of fast axon transport by activating an enzyme called JNK that can inhibit these transport proteins.

Brady said this is the first proposed mechanism for polyQ diseases that explains why only nerve cells die and why the terminals die before the cell body. The link to the activation of the JNK enzyme suggests a new therapeutic target that might limit, delay or perhaps prevent progressive neurodegeneration, the researchers conclude.

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Source:University of Illinois at Chicago


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