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 journal › Journal article › Research › peer-review
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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