CNS Regeneration by Jeffrey Kordower, Mark H. Tuszynski

By Jeffrey Kordower, Mark H. Tuszynski

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In the CNS, we are just beginning to see some hope that regeneration through the native CNS environment may be possible some day. However, the amount of regeneration that has been achieved so far is still insufficient to restore function. It is hoped that future research will provide insights into better methods to activate neurons’ intrinsic growth state, to overcome inhibitory signals without interfering with axon guidance, and to steer axons to their appropriate destinations. At one time, the mere possibility of getting axons to grow in the CNS seemed remote: now that this is becoming a reality, we need to get ready for the next set of challenges.

2003). , BDNF, CNTF, GDNF, or bFGF. , 2000). When isolated by column chromatography and sequenced, the principal macrophage-derived growth factor was identified as Oncomodulin. Oncomodulin is a small Ca2+ protein not previously known to act as a trophic factor and not related to other identified trophic factors. Oncomodulin binds with high affinity to a cell-surface receptor on RGCs and stimulates more extensive outgrowth than any other growth factor tested. , 1998). Immune-depletion of oncomodulin from macrophage-conditioned media eliminated the axon-promoting activity of the conditioned media.

Combining macrophage activation with BDNF augments RGC survival to very high levels (Pernet and Di Polo, 2006). ROLE OF MICROGLIA Microglia, the resident immune cells of the nervous system, are distributed in a regular mosaic array in the ganglion cell layer and inner nuclear layer of the retina and become activated a few days after optic nerve injury (Thanos, 1992; Zhang and Tso, 2003). , 2007). Their role in phagocytosing dying RGCs is readily demonstrated by dyetransfer studies (Thanos, 1992).

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