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Injury-related dynamic myelin/oligodendrocyte axon-outgrowth inhibition in the central nervous system.

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Title: Injury-related dynamic myelin/oligodendrocyte axon-outgrowth inhibition in the central nervous system.
Authors: Schwab JM (AUTHOR), Failli V (AUTHOR), Chedotal A (AUTHOR), Schwab, Jan M (AUTHOR), Failli, Vieri (AUTHOR), Chédotal, Alain (AUTHOR)
Source: Lancet. 6/11/2005, Vol. 365 Issue 9476, p2055-2057. 3p.
Abstract: Context: By contrast with the glial scar, myelin was considered a constitutive static inhibitory barrier unreactive to lesions in the central nervous system (CNS). However, recent results suggest considerable add-on inhibition of myelin as a result of CNS injury. Furthermore, catastrophic events cause morphological and biochemical changes in the axon itself. This results in the accumulation of cytoskeleton components and intraaxonal transported proteins paralleled by extensive membrane remodelling at the axonal tip (a process called axotomy) which might modify the axonal response to its inhibitory environment. Starting Point: Ji-Eun Kim and colleagues recently reported an axonal subpopulation with a different capacity to respond to myelin inhibitors (Neuron 2004; 44: 439-51). Axonal specificity but also evidence for injury reactivity summarised here challenges our understanding of axon-growth inhibition in the injured CNS. This might be due to (i) qualitative and quantitative enrichment of the periaxonal environment by myelin/oligodendrocytes, (ii) increased axonal sensitivity to its inhibitory environment, and (iii) axons and lesion-induced, altered axonal signalling. WHERE NEXT? Postlesional reactive inhibition of myelin or the oligodendrocyte necessitates the development of novel screening approaches and therapeutic agents to promote axonal regeneration. Moreover, we need to improve our understanding of the pathophysiology of the lesion to find more efficient experimental strategies to restore neurological function. [ABSTRACT FROM AUTHOR]
Copyright of Lancet is the property of Lancet and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Injury-related dynamic myelin/oligodendrocyte axon-outgrowth inhibition in the central nervous system.
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  Data: <searchLink fieldCode="AR" term="%22Schwab+JM%22">Schwab JM</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Failli+V%22">Failli V</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Chedotal+A%22">Chedotal A</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Schwab%2C+Jan+M%22">Schwab, Jan M</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Failli%2C+Vieri%22">Failli, Vieri</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Chédotal%2C+Alain%22">Chédotal, Alain</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22Lancet%22">Lancet</searchLink>. 6/11/2005, Vol. 365 Issue 9476, p2055-2057. 3p.
– Name: Abstract
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  Data: <bold>Context: </bold>By contrast with the glial scar, myelin was considered a constitutive static inhibitory barrier unreactive to lesions in the central nervous system (CNS). However, recent results suggest considerable add-on inhibition of myelin as a result of CNS injury. Furthermore, catastrophic events cause morphological and biochemical changes in the axon itself. This results in the accumulation of cytoskeleton components and intraaxonal transported proteins paralleled by extensive membrane remodelling at the axonal tip (a process called axotomy) which might modify the axonal response to its inhibitory environment. <bold>Starting Point: </bold>Ji-Eun Kim and colleagues recently reported an axonal subpopulation with a different capacity to respond to myelin inhibitors (Neuron 2004; 44: 439-51). Axonal specificity but also evidence for injury reactivity summarised here challenges our understanding of axon-growth inhibition in the injured CNS. This might be due to (i) qualitative and quantitative enrichment of the periaxonal environment by myelin/oligodendrocytes, (ii) increased axonal sensitivity to its inhibitory environment, and (iii) axons and lesion-induced, altered axonal signalling. WHERE NEXT? Postlesional reactive inhibition of myelin or the oligodendrocyte necessitates the development of novel screening approaches and therapeutic agents to promote axonal regeneration. Moreover, we need to improve our understanding of the pathophysiology of the lesion to find more efficient experimental strategies to restore neurological function. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: <i>Copyright of Lancet is the property of Lancet and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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              Text: 6/11/2005
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