Chapter 24 Increasing plasticity and functional recovery of the lesioned spinal cord

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Abstract

In vitro assays have been shown that adult CNS tissue, in particular oligodendrocytes and myelin, contains several molecular constituents (Nogo-A/NI-220, MAG, several proteoglycans) which exert neurite growth inhibitory activity. Elimination of oligodendrocytes or myelin, or application of antibodies against some of these constituents enhance regenerative growth and compensatory sprouting of lesioned ans unlesioned fiber tracts in spinal cord and brain. Enhanced growth of paralleled by various degrees of functional recovery.

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      Edema, lipid peroxidation, inflammation and excitotoxicity cause oligodendroglial death and demyelination of surviving axons (Sekhon and Fehlings, 2001). Distal axons subsequently degenerate, with corollary proximal axons unable to grow through the glial scar due to inhibitory myelin fragments within the lesion site (Schwab, 2002; Fawcett, 2006). Approaches that address this to increase anatomic plasticity include the enzyme Chondroitinase ABC (ChABC) to degrade the gliotic scar and implanting scaffolds or olfactory ensheathing cells (OECs) to guide axons into and through the lesion (Busch and Silver, 2007; Rowland et al., 2008).

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