The re-expression of the homeodomain transcription factor Gtx during remyelination of experimentally induced demyelinating lesions in young and old rat brain

Sim, Fraser J.; Hinks, G.L.; Franklin, R. J. M.

doi:10.1016/s0306-4522(00)00252-9

Cited by 58 publications

(58 citation statements)

References 32 publications

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“…1c,d). The animals were left to survive for 14 and 28 d, at which time remyelination in this model is complete (Woodruff and Franklin, 1999;Sim et al, 2000). To quantify remyelination, we determined the ratio of MBP, a major component of myelin sheaths, relative to ␤2-MG mRNA expression by RT-qPCR on total RNA extracted from laser-capture microdissected lesion tissue (Fig.…”

Section: Resultsmentioning

confidence: 99%

Myelin Impairs CNS Remyelination by Inhibiting Oligodendrocyte Precursor Cell Differentiation

Kotter¹,

Li²,

Zhao³

et al. 2006

J. Neurosci.

673

570

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Demyelination in the adult CNS can be followed by extensive repair. However, in multiple sclerosis, the differentiation of oligodendrocyte lineage cells present in demyelinated lesions is often inhibited by unknown factors. In this study, we test whether myelin debris, a feature of demyelinated lesions and an in vitro inhibitor of oligodendrocyte precursor differentiation, affects remyelination efficiency. Focal demyelinating lesions were created in the adult rat brainstem, and the naturally generated myelin debris was augmented by the addition of purified myelin. After quantification of myelin basic protein mRNA expression from lesion material obtained by laser capture microdissection and supported by histological data, we found a significant impairment of remyelination, attributable to an arrest of the differentiation and not the recruitment of oligodendrocyte precursor cells. These data identify myelin as an inhibitor of remyelination as well as its well documented inhibition of axon regeneration.

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Section: Resultsmentioning

confidence: 99%

Myelin Impairs CNS Remyelination by Inhibiting Oligodendrocyte Precursor Cell Differentiation

Kotter¹,

Li²,

Zhao³

et al. 2006

J. Neurosci.

673

570

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“…Together (5) these changes would effectively "disconnect" parts of the aging brain and lead to cognitive impairments There is growing evidence that remyelination failure is also a significant contributing mechanism of age-related WM disturbances. Remyelination efficiency decreases with age (Gilson and Blakemore 1993;Shields et al 1999;Sim et al 2000). This decline in remyelination efficiency has been linked to impairments in oligodendrocyte progenitor cell (OPC) recruitment and differentiation into myelinating oligodendrocytes (OLs; Sim et al 2002;Peters and Sethares 2002;Franklin et al 2002;Ando et al 2003;Chari et al 2003;Woodruff et al 2004;Rist and Franklin 2008).…”

Section: Mechanisms Of Wm Changes During Normative Agingmentioning

confidence: 99%

Age-related changes in human and non-human primate white matter: from myelination disturbances to cognitive decline

Kohama

Rosene

Sherman

2011

AGE

121

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The cognitive decline associated with normal aging was long believed to be due primarily to decreased synaptic density and neuron loss. Recent studies in both humans and non-human primates have challenged this idea, pointing instead to disturbances in white matter (WM) including myelin damage. Here, we review both cross-sectional and longitudinal studies in humans and non-human primates that collectively support the hypothesis that WM disturbances increase with age starting at middle age in humans, that these disturbances contribute to age-related cognitive decline, and that age-related WM changes may occur as a result of free radical damage, degenerative changes in cells in the oligodendrocyte lineage, and changes in microenvironments within WM.

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“…To understand the functional role of the Notch1 pathway in remyelination we have taken advantage of the contribution that delayed OPC differentiation makes to age-associated delay in remyelination (Sim et al, 2000). We hypothesized that Jagged1 expression by demyelinated axons may be prolonged in older animals, delaying differentiation of Notch1-expressing OPCs.…”

Section: Introductionmentioning

confidence: 99%

Notch1 and Jagged1 are expressed after CNS demyelination, but are not a major rate-determining factor during remyelination

Stidworthy

Genoud²,

Li³

et al. 2004

Brain

148

113

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The re-expression of the homeodomain transcription factor Gtx during remyelination of experimentally induced demyelinating lesions in young and old rat brain

Cited by 58 publications

References 32 publications

Myelin Impairs CNS Remyelination by Inhibiting Oligodendrocyte Precursor Cell Differentiation

Myelin Impairs CNS Remyelination by Inhibiting Oligodendrocyte Precursor Cell Differentiation

Age-related changes in human and non-human primate white matter: from myelination disturbances to cognitive decline

Notch1 and Jagged1 are expressed after CNS demyelination, but are not a major rate-determining factor during remyelination

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