Role of tubulin post-translational modifications in peripheral neuropathy

Peripheral neuropathy is a common disorder that results from nerve damage in the periphery. The degeneration of sensory axon terminals leads to changes or loss of sensory functions, often manifesting as debilitating pain, weakness, numbness, tingling, and disability. The pathogenesis of most peripheral neuropathies remains to be fully elucidated. Cumulative evidence from both early and recent studies indicates that tubulin damage may provide a common underlying mechanism of axonal injury in various peripheral neuropathies. In particular, tubulin post-translational modifications have been recently implicated in both toxic and inherited forms of pe-ripheral neuropathy through regulation of axonal transport and mitochondria dynamics. This knowledge forms a new area of investigation with the potential for developing therapeutic strategies to prevent or delay peripheral neuropathy by restoring tubulin homeostasis.

Automated summary

Peripheral neuropathy is a common disorder resulting from nerve damage in the periphery. The degeneration of sensory axon terminals leads to changes in sensory functions, causing pain, weakness, numbness, tingling, and disability. Tubulin damage has been identified as a potential underlying mechanism for various peripheral neuropathies, and post-translational modifications of tubulin have been implicated in the regulation of axonal transport and mitochondria dynamics.