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Soluble Nogo-A, an inhibitor of axonal regeneration, as a biomarker for multiple sclerosis

From the Department of Neurology (A.J., M.M., K.S.), Medical University of Lodz, Poland; and Departments of Pathology (Neuropathology) (C.S.R.), Neurology (C.S.R.), and Neuroscience (C.S.R.), Albert Einstein College of Medicine, Bronx, NY.

Address correspondence and reprint requests to Dr. Krzysztof Selmaj, Department of Neurology, Medical University of Lodz, 22, Kopciskiego Street, 90-153 Lodz, Poland; e-mail: kselmaj{at}afazja.am.lodz.pl

Background: CNS axons display a poor regenerative response to injury. In multiple sclerosis (MS), failure of damaged axons to regenerate may be a major factor underlying non-reversible neurologic dysfunction. Nogo is a development-related molecule inhibiting axonal regeneration and is a major component of CNS myelin.

Methods: CSF from 114 patients with remitting relapsing MS (RR-MS) and secondary progressive MS (SP-MS) and 153 controls, as well as CNS tissue from 3 patients with MS and 2 controls, were used for this study.

Results: We found soluble 20 kDa Nogo-A product in 96% (110/114) of CSF samples from patients with MS compared with 0/18 from meningo-encephalomyelitis, 0/125 from control subjects with other neurologic diseases, and 0/10 from CNS autoimmune diseases. Nogo-A products were present both in RR-MS and SP-MS, as well as in early cases of the disease, but not in neuromyelitis optica. The same Nogo A product was detected in CNS tissue from all patients with MS but not in control CNS tissue.

Conclusion: Soluble Nogo-A may be specific for the CSF of patients with multiple sclerosis and its presence may predict failure of axonal regeneration within the CNS.

Supported by KBN grants 3PO5A 03123, 3PO5A 04425; MU grant 502-11-259; by grants HHS NS 08952 and NS 11920; and NMSS RG 1001-K-11.

Disclosure: The authors report no conflicts of interest.

Received April 14, 2006. Accepted in final form October 6, 2006.

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