Nogo signaling and non-physical injury-induced nervous system pathology
✍ Scribed by Felicia Yu Hsuan Teng; Bor Luen Tang
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 212 KB
- Volume
- 79
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Abstract
The Nogo gene products were described first as myelin‐associated inhibitors that prevent neuronal regeneration upon injury. Recent findings have also implicated Nogo in several neuronal pathologies that are not induced by physical injury. Nogo‐A may be an important determinant of autoimmune demyelinating diseases, as active immunization with Nogo‐A fragments attenuates the symptoms of experimental autoimmune encephalomyelitis (EAE). Nogo‐A levels are elevated markedly in hippocampal neurons of patients with temporal lobe epilepsy (TLE), in brain and muscle of patients with amyotrophic lateral sclerosis (ALS), and in schizophrenic patients. Concrete evidence for a direct role of Nogo‐A in the latter neuropathies is not yet available, but such a role is logically in line with new findings associated with localization of Nogo‐A and Nogo–Nogo‐66 receptor (NgR)‐mediated signaling. We speculate on possible linkages between the effect of aberrant elevation of Nogo levels and the signaling consequences that could lead to nervous system pathology. © 2004 Wiley‐Liss, Inc.