ReviewSpinal Cord Repair: Strategies to Promote Axon Regeneration
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Cited by (74)
Effects of bacterial melanin on motor recovery and regeneration after unilateral destruction of Substantia Nigra pars compacta in rats
2014, NeuropeptidesCitation Excerpt :Research publications of key researchers in the field of neurobiology consider in detail the mechanisms of axon regeneration in mammalian central nervous system (Brosamle and Schwab, 1996), regeneration in the spinal cord (Bregman, 1998), formation of glial cicatrix (Fawcett and Asher, 1999), neuroglia activation in the damaged brain (Raivich et al., 1996), strategies to assist and maintain axonal regeneration (McKerracher, 2001).
Neuroprotective action of bacterial melanin in rats after corticospinal tract lesions
2012, PathophysiologyCitation Excerpt :The investigations of the past two decades have radically changed specialists’ notion on inability of neurons of the central nervous system (CNS) to regenerate [11]. Key researchers in the field of neurobiology in their literary reviews consider in detail mechanisms of axon regeneration in mammalians’ CNS [12], regeneration in the spinal cord [13], formation of glial cicatrix [14], neuroglia activation in the damaged brain [15], strategy of axon regeneration maintenance or assistance [16], regeneration of peripheral nerve subjected to damage [17]. These reviews also dwell upon the possibilities of application of physiologically active compounds regulating cascade of processes involved in nervous tissue regeneration and promoting optimization of this process.
Scar ablation combined with LP/OEC transplantation promotes anatomical recovery and P0-positive myelination in chronically contused spinal cord of rats
2011, Brain ResearchCitation Excerpt :Although studies have shown neurons with axonotmesis in the chronically injured spinal cord still maintain the ability to regenerate, the glial scar effectively blocks the elongation of regenerating axons (Bareyre, 2008; Houle, 1991; Kobayashi et al., 1997; Siebert et al., 2010; Silver and Miller, 2004; Steeves and Zwimpfer, 1997). The cessation of axonal elongation via glial inhibition is therefore thought to be behind the failure of functional recovery in a chronically injured spinal cord (Bradbury and Carter, 2011; Davies et al., 1997; Houle and Reier, 1988; McKerracher, 2001; Silver and Miller, 2004). Several studies have suggested that significant axonal growth into the graft requires the removal of inhibitory chondroitin sulfate proteoglycans (CSPG) and astrocytic scar tissue from the lesion site prior to transplantation (Bradbury et al., 2002; Carter et al., 2011; Garcia-Alias et al., 2009; Houle and Tessler, 2003; Hulsebosch, 2002; Tom et al., 2009).
Satellite glia not DRG neurons constitutively activate EGFR but EGFR inactivation is not correlated with axon regeneration
2010, Neurobiology of DiseaseCitation Excerpt :After dorsal column (DC) lesions, the growth of all centrally projecting dorsal root ganglion neuron (DRGN) axons is arrested at the injury site by both CNS myelin-/scar-derived axon growth inhibitory ligands (e.g. Nogo-A, myelin associated glycoprotein (MAG), chondroitin sulphate proteoglycan (CSPG), ephrins and semaphorins) and a limited availability of neurotrophic factors required to maintain DRGN survival and promote axon regeneration (Hunt et al., 2002; Sandvig et al., 2004; Fournier et al., 2002; McKerracher, 2001; McKerracher and Winton, 2002; Hou et al., 2008; Fabes et al., 2007; Du et al., 2007; Berry et al., 2008).
AAV-mediated inhibition of ULK1 promotes axonal regeneration in the central nervous system in vitro and in vivo
2021, Cell Death and Disease