CONCLUSION

Axonal damage is a prominent feature of MS responsible for long-term disability and functional deficits in those afflicted with the disease. In this review we outlined biochemical, clinical, neuropathological, and neuroimaging evidence in support of neurodegeneration as a direct consequence of demyelination or as an independently occurring concurrent event. Future studies should continue to address the molecular changes that occur to both axons and myelin in order to determine the specific sequence of events underlying the disease pathogenesis of MS. Novel therapies addressing the neurodegenerative component of the disease may hold clues for halting its progression and promoting functional recovery in those afflicted with MS.

Acknowledgments

This work is funded in part by a grant from the National Multiple Sclerosis Foundation (NMSS RG-4134/A9) and American Recovery and Reinvestment Act Funds (R01-NS42925-07S1 and NS42925-08) to PC.

Footnotes

DISCLOSURES

Potential conflict of interest: Nothing to report.

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