Chapter 24 Increasing plasticity and functional recovery of the lesioned spinal cord
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2012, Experimental NeurologyCitation Excerpt :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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