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

  title={Pattern-specific loss of aquaporin-4 immunoreactivity distinguishes neuromyelitis optica from multiple sclerosis.},
  author={Shanu Faerch Roemer and Joseph E. Parisi and Vanda A. Lennon and Eduardo E. Benarroch and Hans Lassmann and Wolfgang Bruck and Raul N Mandler and Brian G. Weinshenker and Sean J. Pittock and Dean M. Wingerchuk and Claudia F. Lucchinetti},
  journal={Brain : a journal of neurology},
  volume={130 Pt 5},
Neuromyelitis optica (NMO) is an inflammatory demyelinating disease that typically affects optic nerves and spinal cord. Its pathogenic relationship to multiple sclerosis (MS) is uncertain. Unlike MS, NMO lesions are characterized by deposits of IgG and IgM co-localizing with products of complement activation in a vasculocentric pattern around thickened hyalinized blood vessels, suggesting a pathogenic role for humoral immunity targeting an antigen in the perivascular space. A recently… 

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Antibody to aquaporin-4 in the long-term course of neuromyelitis optica

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Neuromyelitis optica should be classified as an astrocytopathic disease rather than a demyelinating disease

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Neuromyelitis optica pathogenesis and aquaporin 4

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Loss of aquaporin-4 in active perivascular lesions in neuromyelitis optica: a case report.

The findings suggest that astrocytic impairment associated with humoral immunity against AQP4 may be primarily involved in the lesion formation of N MO, and that the pathomechanisms of NMO are different from those of MS in which demyelination is the primary pathology.

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

The distribution of NMO-characteristic brain lesions corresponds to sites of high AQP4 expression in mammalian brain, and recurring and distinctive magnetic resonance imaging abnormalities in the hypothalamic and periventricular areas that corresponded to brain regions ofhigh AQP 4 expression are observed.

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

It is shown that NMO-IgG binds selectively to the aquaporin-4 water channel, a component of the dystroglycan protein complex located in astrocytic foot processes at the blood-brain barrier, which may represent the first example of a novel class of autoimmune channelopathy.

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

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

The extent of complement activation, eosinophilic infiltration and vascular fibrosis observed in the Devic NMO cases is more prominent compared with that in prototypic multiple sclerosis, and supports a role for humoral immunity in the pathogenesis of NMO.

Enhanced expression of aquaporin 4 in human brain with inflammatory diseases

Investigation of AQP4 expression in autopsied brains with multiple sclerosis, HIVE, human immunodeficiency virus encephalitis or progressive multifocal leukoencephalopathy concluded that functions and regulation of AQp4 in human brains are multiple.

Brain abnormalities in neuromyelitis optica.

MRI brain findings in NMO justify revision of diagnostic criteria for NMO to allow for brain involvement, and asymptomatic brain lesions do not exclude the diagnosis of NMO.

Revised diagnostic criteria for neuromyelitis optica

Revised diagnostic criteria for definite neuromyelitis optica (NMO) that require optic neuritis, myelitis, and at least two of three supportive criteria: MRI evidence of a contiguous spinal cord lesion 3 or more segments in length, onset brain MRI nondiagnostic for multiple sclerosis, or NMO-IgG seropositivity.

The clinical course of neuromyelitis optica (Devic’s syndrome)

Clinical, laboratory, and imaging features generally distinguish neuromyelitis optica from MS, and patients with relapsing optic neuritis and myelitis may have neuromyeliitis opticas rather than MS.

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

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