The astrocyte in multiple sclerosis revisited

  title={The astrocyte in multiple sclerosis revisited},
  author={Celia F. Brosnan and Cedric S. Raine},
Among the constituent cell types of the multiple sclerosis (MS) plaque, the astrocyte has been the least considered as a player in the pathogenesis of the lesion. Traditionally, it has been assigned a secondary scarring role with little or no role in lesion formation or repair. However, the recent upsurge of interest in the demyelinating condition neuromyelitis optica (NMO) has resulted in NMO being identified as the first disease of myelin in which primary damage to astrocytes, resulting from… 
Multiple Sclerosis: Destruction and Regeneration of Astrocytes in Acute Lesions
Loss and recovery of astrocytes in new MS lesions may be as important as myelin loss as a cause of conduction block responsible for symptoms in patients with relapsing and remitting and secondary progressive MS.
Multiple sclerosis: Lessons from molecular neuropathology
  • H. Lassmann
  • Biology, Psychology
    Experimental Neurology
  • 2014
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Tissue remodeling in periplaque regions of multiple sclerosis spinal cord lesions
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Continual study into the initiation, evolution, and resolution of the multiple sclerosis lesion offers the therapeutic opportunities to enhance the beneficial capabilities of these cells while limiting their destructive effects.
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Neuroinflammation is the coordinated response of the central nervous system (CNS) to threats to its integrity posed by a variety of conditions, including autoimmunity, pathogens and trauma. Activated
Inflammatory demyelinating diseases of the central nervous system
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Myelin phagocytosis by astrocytes after myelin damage promotes lesion pathology
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Neuromyelitis optica: a demyelinating disease characterized by acute destruction and regeneration of perivascular astrocytes
The findings raise the possibility that demyelination in MS may be a bystander effect of an astrocyte lesion, i.e. that MS is not a disease primarily of myelin and oligodendrocytes, and add to experimental evidence that the antibody is pathogenic.
Astrocytes—Friends or foes in multiple sclerosis?
In multiple sclerosis, the presence of demyelinating plaques has concentrated researchers' minds on the role of the oligodendrocyte in its pathophysiology, and recent reports on the dual role of astrocytes are reviewed to try to provide a cogent view of astracytes in the pathology of MS.
Astrocyte‐associated axonal damage in pre‐onset stages of experimental autoimmune encephalomyelitis
Significantly, it is shown that, in common with a growing number of neurodegenerative conditions, the pathology of murine EAE is characterized by early active contribution from astrocytes, which marks a change in the understanding of the role of astroCytes in MS pathogenesis and has important implications for the development of neuroprotective strategies.
Multiple sclerosis. Oligodendrocyte survival and proliferation in an active established lesion.
The findings support the notions that there is no selective depletion of oligodendrocytes either during or shortly following central nervous system demyelination in multiple sclerosis, and that the myelin sheath is the primary target.
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Recent data supporting the idea that astrocytes play a complex role in the regulation of CNS autoimmunity are summarized.
Multiple Sclerosis: A Role for Astroglia in Active Demyelination Suggested by Class II MHC Expression and Ultrastructural Study
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Loss of aquaporin 4 in lesions of neuromyelitis optica: distinction from multiple sclerosis.
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Overcoming remyelination failure in multiple sclerosis and other myelin disorders
Immunology of multiple sclerosis.
Recent data suggesting an interaction of T and B cells, as well as serum and CSF proteins including complement and anti-myelin/oligodendrocyte antibodies, in the pathogenesis of MS and EAE are discussed.
Astrogliosis in EAE spinal cord: Derivation from radial glia, and relationships to oligodendroglia
Observations support the hypothesis that necrosis contributes to oligodendroglial loss early in the course of EAE, and accumulation of EGFP+ cells accumulated amongst hypertrophic astroglia at the margins of the lesions, while the lesions themselves remained depleted of oligodENDroglia, suggesting that migration of oligoendrocyte lineage cells into the lesions was retarded by the intense perilesional gliosis.