Role of tubulin post-translational modifications in peripheral neuropathy
Maria Elena Pero1, Farihah Chowdhury2, Francesca Bartolini2
1Department of Pathology and Cell Biology, Columbia University, New York, USA; Department of Veterinary Medicine and Animal Production, University of Naples Federico II, Italy.
Abstract:
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 peripheral 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.
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