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suck abstract from ncbi


10.1016/j.expneurol.2016.04.007

http://scihub22266oqcxt.onion/10.1016/j.expneurol.2016.04.007
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C5010970!5010970 !27079997
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suck abstract from ncbi


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pmid27079997
      Exp+Neurol 2016 ; 283 (Pt B ): 573-80
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  • Promoting peripheral myelin repair #MMPMID27079997
  • Zhou Y ; Notterpek L
  • Exp Neurol 2016[Sep]; 283 (Pt B ): 573-80 PMID27079997 show ga
  • Compared to the central nervous system (CNS), peripheral nerves have a remarkable ability to regenerate and remyelinate. This regenerative capacity to a large extent is dependent on and supported by Schwann cells, the myelin-forming glial cells of the peripheral nervous system (PNS). In a variety of paradigms, Schwann cells are critical in the removal of the degenerated tissue, which is followed by remyelination of newly-regenerated axons. This unique plasticity of Schwann cells has been the target of myelin repair strategies in acute injuries and chronic diseases, such as hereditary demyelinating neuropathies. In one approach, the endogenous regenerative capacity of Schwann cells is enhanced through interventions such as exercise, electrical stimulation or pharmacological means. Alternatively, Schwann cells derived from healthy nerves, or engineered from different tissue sources have been transplanted into the PNS to support remyelination. These transplant approaches can then be further enhanced by exercise and/or electrical stimulation, as well as by the inclusion of biomaterial engineered to support glial cell viability and neurite extension. Advances in our basic understanding of peripheral nerve biology, as well as biomaterial engineering, will further improve the functional repair of myelinated peripheral nerves.
  • |Animals [MESH]
  • |Demyelinating Diseases/*pathology/physiopathology [MESH]
  • |Humans [MESH]
  • |Myelin Sheath/*physiology [MESH]
  • |Nerve Regeneration/*physiology [MESH]
  • |Neuroglia/physiology [MESH]


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