Thursday, 6 September 2012

Research: A way to slow down nerve damage


Protein tyrosine phosphatase receptor type Z (Ptprz) is widely expressed in the mammalian central nervous system and has been suggested to regulate oligodendrocyte survival and differentiation. We investigated the role of Ptprz in oligodendrocyte remyelination after acute, toxin-induced demyelination in Ptprz null mice. We found neither obvious impairment in the recruitment of oligodendrocyte precursor cells, astrocytes, or reactive microglia/macrophage to lesions nor a failure for oligodendrocyte precursor cells to differentiate and remyelinate axons at the lesions. However, we observed an unexpected increase in the number of dystrophic axons by 3 days after demyelination, followed by prominent wallerian degeneration by 21 days in the Ptprz-deficient mice. Moreover, quantitative gait analysis revealed a deficit of locomotor behavior in the mutant mice, suggesting increased vulnerability to axonal injury. We propose that Ptprz is necessary to maintain central nervous system axonal integrity in a demyelinating environment and may be an important target of axonal protection in inflammatory demyelinating diseases, such as multiple sclerosis 
Receptor-type tyrosine-protein phosphatase zeta also known as phosphacan which is found n the remyelinating oligodendrocytes of multiple sclerosis. In mice that lack this enzymne it appears that nerves are more likely to show damage following demyelination. There was enhanced Wallerian degeneration is a process that results when a nerve fibre is cut or crushed, in which the part of the axon separated from the neuron's cell body degenerates below the site of the injury. This suggests that if  Receptor-type tyrosine-protein phosphatase zeta function can be enhanced then it may help in slowing damage to nerves that could be useful in slowing progression.

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