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New component of the 'brakes' on nerve regeneration found

chinery within neurons. Also, they found that treating neurons with a nonfunctional version of TAJ/TROY abolished neurons' response to the "braking" molecules produced by myelin and encouraged neuron growth.

"Given the limited expression of p75, the discovery of TAJ function is an important step for understanding the regulation of axon regeneration," wrote Mi and colleagues.

Wrote Park and colleagues, "The implication that more than one TNF receptor member may be involved in myelin inhibition adds a new level of complexity to designing therapeutic strategies for treating CNS injury." They cited studies showing that TNF receptors are expressed in many types of cells in the CNS and are intimately involved in inflammatory responses that also play a role--perhaps harmful, perhaps beneficial to regeneration or recovery--in regulating response to injury. "Further characterization of the underlying mechanisms of these findings and their relation to myelin inhibition may provide important insights into designing therapeutic strategies to block myelin inhibition and cell death in the context of CNS injury," they wrote.

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Jong Bae Park, Glenn Yiu, Shinjiro Kaneko, Jing Wang, Jufang Chang, and Zhigang He: "A TNF Receptor Family Member, TROY, Is a Coreceptor with Nogo Receptor in Mediating the Inhibitory Activity of Myelin Inhibitors"

Zhaohui Shao, Jeffrey L. Browning, Xinhua Lee, Martin L. Scott, Sveltlana Shulga-Morskaya, Norm Allaire, Greg Thill, Melissa Levesque, Dinah Sah, John M. McCoy, Beth Murray, Vincent Jung, R. Blake Pepinsky, and Sha Mi: "TAJ/TROY, an Orphan TNF Receptor Family Member, Binds Nogo-66 Receptor 1 and Regulates Axonal Regeneration"


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Source:Cell Press


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