Schwann cells keep axons healthy

Schwann cells keep axons healthy

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Access through your institution Buy or subscribe Charcot-Marie-Tooth disease 1A (CMT1A) is an inherited neuropathy caused by duplication of the gene encoding peripheral myelin protein 22 (PMP22). In this study, _PMP22_ duplication in rodents caused defects in Schwann cell differentiation in early postnatal development, which persisted into adulthood. This abnormal Schwann cell phenotype could be rescued by axonal overexpression of neuregulin-1 (NRG1) or by treatment with soluble NRG1 in early postnatal stages. These data suggest that there is a temporal window for correct Schwann cell differentiation that is vital to prevent the neuropathy observed in CMT1A. This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Subscribe to this journal Receive 12 print issues and online access $189.00 per year only $15.75 per issue Learn more Buy this article * Purchase on SpringerLink * Instant access to full article PDF Buy now Prices may be subject to local taxes which are calculated during checkout ADDITIONAL ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support REFERENCES * Fledrich, R. et al. Soluble neuregulin-1 modulates disease pathogenesis in rodent models of Charcot-Marie-Tooth disease 1A. _Nature Med._ http://dx.doi.org/10.1038/nm.3664 (2014) Download references Authors * Sian Lewis View author publications You can also search for this author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Lewis, S. Schwann cells keep axons healthy. _Nat Rev Neurosci_ 15, 632 (2014). https://doi.org/10.1038/nrn3831 Download citation * Published: 19 September 2014 * Issue Date: October 2014 * DOI: https://doi.org/10.1038/nrn3831 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable link Sorry, a shareable link is not currently available for this article. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative

Access through your institution Buy or subscribe Charcot-Marie-Tooth disease 1A (CMT1A) is an inherited neuropathy caused by duplication of the gene encoding peripheral myelin protein 22


(PMP22). In this study, _PMP22_ duplication in rodents caused defects in Schwann cell differentiation in early postnatal development, which persisted into adulthood. This abnormal Schwann


cell phenotype could be rescued by axonal overexpression of neuregulin-1 (NRG1) or by treatment with soluble NRG1 in early postnatal stages. These data suggest that there is a temporal


window for correct Schwann cell differentiation that is vital to prevent the neuropathy observed in CMT1A. This is a preview of subscription content, access via your institution ACCESS


OPTIONS Access through your institution Subscribe to this journal Receive 12 print issues and online access $189.00 per year only $15.75 per issue Learn more Buy this article * Purchase on


SpringerLink * Instant access to full article PDF Buy now Prices may be subject to local taxes which are calculated during checkout ADDITIONAL ACCESS OPTIONS: * Log in * Learn about


institutional subscriptions * Read our FAQs * Contact customer support REFERENCES * Fledrich, R. et al. Soluble neuregulin-1 modulates disease pathogenesis in rodent models of


Charcot-Marie-Tooth disease 1A. _Nature Med._ http://dx.doi.org/10.1038/nm.3664 (2014) Download references Authors * Sian Lewis View author publications You can also search for this author


inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Lewis, S. Schwann cells keep axons healthy. _Nat Rev Neurosci_ 15, 632 (2014).


https://doi.org/10.1038/nrn3831 Download citation * Published: 19 September 2014 * Issue Date: October 2014 * DOI: https://doi.org/10.1038/nrn3831 SHARE THIS ARTICLE Anyone you share the


following link with will be able to read this content: Get shareable link Sorry, a shareable link is not currently available for this article. Copy to clipboard Provided by the Springer


Nature SharedIt content-sharing initiative