Glia Disease and Repair-Remyelination

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Glia Disease and Repair-Remyelination. / Franklin, Robin J M; Goldman, Steven A.

In: Cold Spring Harbor perspectives in biology, Vol. 7, No. 7, a020594, 07.2015, p. 1-28.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Franklin, RJM & Goldman, SA 2015, 'Glia Disease and Repair-Remyelination', Cold Spring Harbor perspectives in biology, vol. 7, no. 7, a020594, pp. 1-28. https://doi.org/10.1101/cshperspect.a020594

APA

Franklin, R. J. M., & Goldman, S. A. (2015). Glia Disease and Repair-Remyelination. Cold Spring Harbor perspectives in biology, 7(7), 1-28. [a020594]. https://doi.org/10.1101/cshperspect.a020594

Vancouver

Franklin RJM, Goldman SA. Glia Disease and Repair-Remyelination. Cold Spring Harbor perspectives in biology. 2015 Jul;7(7):1-28. a020594. https://doi.org/10.1101/cshperspect.a020594

Author

Franklin, Robin J M ; Goldman, Steven A. / Glia Disease and Repair-Remyelination. In: Cold Spring Harbor perspectives in biology. 2015 ; Vol. 7, No. 7. pp. 1-28.

Bibtex

@article{da0c1a322b4742babb13edf85f23c600,
title = "Glia Disease and Repair-Remyelination",
abstract = "The inability of the mammalian central nervous system (CNS) to undergo spontaneous regeneration has long been regarded as a central tenet of neurobiology. However, although this is largely true of the neuronal elements of the adult mammalian CNS, save for discrete populations of granular neurons, the same is not true of its glial elements. In particular, the loss of oligodendrocytes, which results in demyelination, triggers a spontaneous and often highly efficient regenerative response, remyelination, in which new oligodendrocytes are generated and myelin sheaths are restored to denuded axons. Yet, remyelination in humans is not without limitation, and a variety of demyelinating conditions are associated with sustained and disabling myelin loss. In this review, we will review the biology of remyelination, including the cells and signals involved; describe when remyelination occurs and when and why it fails and the consequences of its failure; and discuss approaches for therapeutically enhancing remyelination in demyelinating diseases of both children and adults, both by stimulating endogenous oligodendrocyte progenitor cells and by transplanting these cells into demyelinated brain.",
keywords = "Animals, Cell Differentiation, Humans, Mice, Myelin Sheath, Nerve Regeneration, Neurodegenerative Diseases, Neuroglia, Oligodendroglia, Pluripotent Stem Cells, Signal Transduction, Stem Cell Transplantation",
author = "Franklin, {Robin J M} and Goldman, {Steven A}",
note = "Copyright {\textcopyright} 2015 Cold Spring Harbor Laboratory Press; all rights reserved.",
year = "2015",
month = jul,
doi = "10.1101/cshperspect.a020594",
language = "English",
volume = "7",
pages = "1--28",
journal = "Cold Spring Harbor Perspectives in Biology",
issn = "1943-0264",
publisher = "Cold Spring Harbor Laboratory Press",
number = "7",

}

RIS

TY - JOUR

T1 - Glia Disease and Repair-Remyelination

AU - Franklin, Robin J M

AU - Goldman, Steven A

N1 - Copyright © 2015 Cold Spring Harbor Laboratory Press; all rights reserved.

PY - 2015/7

Y1 - 2015/7

N2 - The inability of the mammalian central nervous system (CNS) to undergo spontaneous regeneration has long been regarded as a central tenet of neurobiology. However, although this is largely true of the neuronal elements of the adult mammalian CNS, save for discrete populations of granular neurons, the same is not true of its glial elements. In particular, the loss of oligodendrocytes, which results in demyelination, triggers a spontaneous and often highly efficient regenerative response, remyelination, in which new oligodendrocytes are generated and myelin sheaths are restored to denuded axons. Yet, remyelination in humans is not without limitation, and a variety of demyelinating conditions are associated with sustained and disabling myelin loss. In this review, we will review the biology of remyelination, including the cells and signals involved; describe when remyelination occurs and when and why it fails and the consequences of its failure; and discuss approaches for therapeutically enhancing remyelination in demyelinating diseases of both children and adults, both by stimulating endogenous oligodendrocyte progenitor cells and by transplanting these cells into demyelinated brain.

AB - The inability of the mammalian central nervous system (CNS) to undergo spontaneous regeneration has long been regarded as a central tenet of neurobiology. However, although this is largely true of the neuronal elements of the adult mammalian CNS, save for discrete populations of granular neurons, the same is not true of its glial elements. In particular, the loss of oligodendrocytes, which results in demyelination, triggers a spontaneous and often highly efficient regenerative response, remyelination, in which new oligodendrocytes are generated and myelin sheaths are restored to denuded axons. Yet, remyelination in humans is not without limitation, and a variety of demyelinating conditions are associated with sustained and disabling myelin loss. In this review, we will review the biology of remyelination, including the cells and signals involved; describe when remyelination occurs and when and why it fails and the consequences of its failure; and discuss approaches for therapeutically enhancing remyelination in demyelinating diseases of both children and adults, both by stimulating endogenous oligodendrocyte progenitor cells and by transplanting these cells into demyelinated brain.

KW - Animals

KW - Cell Differentiation

KW - Humans

KW - Mice

KW - Myelin Sheath

KW - Nerve Regeneration

KW - Neurodegenerative Diseases

KW - Neuroglia

KW - Oligodendroglia

KW - Pluripotent Stem Cells

KW - Signal Transduction

KW - Stem Cell Transplantation

U2 - 10.1101/cshperspect.a020594

DO - 10.1101/cshperspect.a020594

M3 - Journal article

C2 - 25986556

VL - 7

SP - 1

EP - 28

JO - Cold Spring Harbor Perspectives in Biology

JF - Cold Spring Harbor Perspectives in Biology

SN - 1943-0264

IS - 7

M1 - a020594

ER -

ID: 162151596