Dissecting demyelination

@article{Miller2007DissectingD,
  title={Dissecting demyelination},
  author={Robert H. Miller and Sha Mi},
  journal={Nature Neuroscience},
  year={2007},
  volume={10},
  pages={1351-1354}
}
The loss of central nervous system myelin and the failure of remyelination by oligodendrocytes contribute to the functional impairment that characterizes diseases such as multiple sclerosis. Why myelin repair fails in multiple sclerosis is currently unclear; however, new understanding of the generation of oligodendrocytes and myelination during development, as well as an increasing understanding of the bases of successful remyelination, are providing new insights and therapeutic targets. We… Expand
View on Nature
ncbi.nlm.nih.gov
82 Citations
Highly Influential Citations
6
Background Citations
47
Methods Citations
2

82 Citations

Citation Type

Citation Type

Mechanisms of remyelination: recent insight from experimental models
TLDR
This review focuses on the molecular mechanisms controlling the differentiation of oligodendrocytes during remyelination, and the function of astrocyte and microglia in animal models of demyelinating diseases. Expand
Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination
TLDR
Current understanding of the processes at issue is summarized, with emphasis upon myelin composition/architecture and oligodendrocyte maturation and differentiation, and avenues being actively pursued to promote remyelination including cytokine-based immune-intervention, antigen-based immunomodulation, and recombinant monoclonal antibodies-induced remYelination. Expand
Enhancing remyelination in disease--can we wrap it up?
TLDR
A model is proposed that may help to provide cues for how remyelination can be therapeutically enhanced in clinical disease and is critically evaluates recent advances in understanding of the biology of oligodendrocyte precursor cells and of the stage-dependent molecular pathology of multiple sclerosis lesions relevant to the regeneration of myelin sheaths. Expand
From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases
TLDR
Recent studies that address the innate repair capabilities of the axon-glia unit from fish to man are discussed and it is proposed that expansion of this research field will help to maintain or enhance spontaneous remyelination in man. Expand
Cells of the oligodendroglial lineage, myelination, and remyelination.
TLDR
The limited remyelination observed in more chronic MS lesions may reflect intrinsic properties of neural cells or extrinsic deterrents, and may indicate why demyelinated axons undergo degeneration more readily. Expand
Remyelination and Multiple Sclerosis: Therapeutic Approaches and Challenges
TLDR
Preclinical and clinical studies on the most promising potential therapies for inducing remyelination will be described, and a promising avenue for protecting axons, reversing neurologic disability and preventing progressive disease in MS is promoted. Expand
rHIgM22 enhances remyelination in the brain of the cuprizone mouse model of demyelination
TLDR
It is demonstrated that treatment with rHIgM22 accelerated remyelination of the demyelinated corpus callosum and enhancing effects were also accompanied by increased differentiation of OPCs into mature oligodendrocytes. Expand
Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned
TLDR
The cuprizone model is reviewed to demonstrate that there is an important crosstalk between astrocytes and microglia and its potential therapeutic relevance for the human disease MS are critically discussed in comparison to other animal models. Expand
Neuroprotection and neuroregeneration in multiple sclerosis
TLDR
Further knowledge about the molecular mechanisms of the repair processes and MS pathophysiology is required to achieve the ultimate goal of a neuroprotective and neuroregenerative treatment in MS. Expand
Dysregulation of the Wnt pathway inhibits timely myelination and remyelination in the mammalian CNS.
TLDR
It is shown that dysregulation of Wnt-beta-catenin signaling in OLPs results in profound delay of both developmental myelination and remyelination, based on findings from APC(Min) mice, which lack one functional copy of the endogenous Wnt pathway inhibitor APC. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 52 REFERENCES
Lessons from oligodendrocyte biology on promoting repair in multiple sclerosis
TLDR
Four areas where recent advances have important implications for remyelination strategies are highlighted, including the pro-myelinogenic factors in the immune response, the extracellular matrix and its integrin receptors, inflammation, and oligodendrocyte precursor cells. Expand
Premyelinating oligodendrocytes in chronic lesions of multiple sclerosis.
TLDR
Understanding the cellular interactions between premyelinating oligodendrocytes, axons, and the microenvironment of lesions of multiple sclerosis may lead to effective strategies for enhancing remyelination. Expand
Failure of Remyelination in the Nonhuman Primate Optic Nerve
TLDR
The present data suggest that the reduced oligodendrocyte progenitor population, the improper activation of oligodendedrocytes at the onset of remyelination in the optic nerve, and possibly, the involvement of astroCytes contribute to the chronicity of the optic nerves lesion. Expand
Glial progenitor-based repair of demyelinating neurological diseases.
TLDR
Given the relative availability and homogeneity of human oligodendrocyte progenitor cells, the disorders of myelin formation and maintenance may be especially compelling targets for cell-based neurologic therapy. Expand
Why does remyelination fail in multiple sclerosis?
TLDR
Why remyelination fails is crucial for devising effective methods by which to enhance it, and as the disease progresses, the numbers of lesions in which demyelinations persists increases, significantly contributing to clinical deterioration. Expand
Impaired remyelination and depletion of oligodendrocyte progenitors does not occur following repeated episodes of focal demyelination in the rat central nervous system.
TLDR
Following recovery from focal, toxin-induced CNS demyelination, the OPC density returned to levels equivalent to those in normal white matter and there was no depletion of OPCs following repeated episodes of focal, toxins-induced brain stem white matter demYelination at the same site. Expand
Axonal transection in the lesions of multiple sclerosis.
TLDR
Transected axons are common in the lesions of multiple sclerosis, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease. Expand
Injection of adult neurospheres induces recovery in a chronic model of multiple sclerosis
TLDR
Adult neural precursor cells promote multifocal remyelination and functional recovery after intravenous or intrathecal injection in a chronic model of multiple sclerosis, both clinically and neurophysiologically. Expand
Repair of demyelinated lesions by transplantation of purified 0-2A progenitor cells
TLDR
These results offer a viable strategy for the manipulation of neural precursor cells which is compatible with attempts to repair damaged CNS tissue by precursor transplants by co-operating growth factors. Expand
Schwann cell precursors: a favourable cell for myelin repair in the Central Nervous System.
TLDR
This work tested whether problems relating to the incompatibility between peripheral glial cells and the CNS glial environment can be avoided by using an earlier stage of the Schwann cell lineage, the SchwANN cell precursor (SCP), and found that these cells share some of the main advantages of Schwann cells without suffering from the disadvantages. Expand
...
1
2
3
4
5
...