Neuromyelitis optica lesions may inform multiple sclerosis heterogeneity debate (Q28276365)

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Ralf Gold

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object named as

Ralf Gold

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author name string

Wolfgang Brück

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Bogdan Popescu

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Claudia F Lucchinetti

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Silva Markovic-Plese

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Imke Metz

A serum autoantibody marker of neuromyelitis optica: distinction from multiple sclerosis

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language of work or name

English

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publication date

September 2012

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published in

Annals of Neurology

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volume

72

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issue

3

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page(s)

385-94

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cites work

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IgG marker of optic-spinal multiple sclerosis binds to the aquaporin-4 water channel

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Loss of aquaporin 4 in lesions of neuromyelitis optica: distinction from multiple sclerosis.

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Pattern-specific loss of aquaporin-4 immunoreactivity distinguishes neuromyelitis optica from multiple sclerosis.

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A role for humoral mechanisms in the pathogenesis of Devic's neuromyelitis optica

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Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination

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Monocyte/macrophage differentiation in early multiple sclerosis lesions.

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Persistence of immunopathological and radiological traits in multiple sclerosis.

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Relapsing and remitting multiple sclerosis: pathology of the newly forming lesion

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Brain magnetic resonance imaging abnormalities in neuromyelitis optica

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Characteristic brain magnetic resonance imaging abnormalities in central nervous system aquaporin-4 autoimmunity.

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A case of cerebral aquaporinopathy

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Supraspinal demyelinating lesions in neuromyelitis optica display a typical astrocyte pathology.

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Clinical characteristics of African Americans vs Caucasian Americans with multiple sclerosis

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Oligoclonal myelin-reactive T-cell infiltrates derived from multiple sclerosis lesions are enriched in Th17 cells.

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Immunoglobulins and complement in postmortem multiple sclerosis tissue

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Neuromyelitis optica brain lesions localized at sites of high aquaporin 4 expression

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Neuromyelitis optica unique area postrema lesions: nausea, vomiting, and pathogenic implications

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Mitochondrial defects in acute multiple sclerosis lesions

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Nitric oxide as a potential pathological mechanism in demyelination: its differential effects on primary glial cells in vitro

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1 reference

Neuromyelitis optica: pathogenicity of patient immunoglobulin in vivo.

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Oligodendrocytes are damaged by neuromyelitis optica immunoglobulin G via astrocyte injury.

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Inflammation induced by innate immunity in the central nervous system leads to primary astrocyte dysfunction followed by demyelination.

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Aquaporin-4 astrocytopathy in Baló’s disease

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Activation of Kainate Receptors Sensitizes Oligodendrocytes to Complement Attack

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Identifiers

DOI

10.1002/ANA.23621

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Consolidated OpenCitations Corpus – April 2017

4436881

4436881

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Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

1 reference