Posts tagged: demyelination

Brain, awy010, Published: 13 February 2018 Robert Wilson Mateusz Makuch Anne-Kathrin Kienzler James Varley Jennifer Taylor Mark Woodhall Jacqueline Palace M Isabel Leite Patrick…

Handb Clin Neurol. 2016;133:377-403. doi: 10.1016/B978-0-444-63432-0.00021-9. Autoimmune AQP4 channelopathies and neuromyelitis optica spectrum disorders. Hinson SR1, Lennon VA1, Pittock SJ2. Abstract Neuromyelitis optica (NMO) spectrum…

? NARCOMS Report-2007 Registry Update Optic Neuritis in Multiple Sclerosis ? Neuromyelitis Optica Dean M. Wingerchuk, MD, MSc, FRCP(C) A Historical Perspective on NMO Neuromyelitis optica (NMO), also known as Devic’s disease, was identified more than one hundred years ago as a severe disorder affecting the spinal cord (causing paralysis) and both optic nerves (causing blindness).

Neuromyelitis optica is an inflammatory demyelinating disease of the central nervous system associated with autoantibodies against the glial water channel protein aquaporin-4. It has recently been reported that immunoglobulin from neuromyelitis optica patients injected peripherally does not cause lesions in naive rats, but only when pre-existing central nervous system inflammation is present

OBJECTIVE: To asses the presence of cortical demyelination in brains of patients with neuromyelitis optica (NMO). NMO is an autoimmune inflammatory demyelinating disease that specifically targets aquaporin-4-rich regions of the CNS. Since aquaporin-4 is highly expressed in normal cortex, we anticipated that cortical demyelination may occur in NMO

BACKGROUND: A serum antibody directed against astrocytes is present in a high proportion of patients with neuromyelitis optica (NMO). The pathogenicity of the antibody is uncertain because no consistent astrocyte lesion is known to occur in NMO

Primary loss and dysfunction of astrocytes may trigger demyelination, as seen in neuromyelitis optica, an inflammatory disease of the central nervous system. In most patients affected by this disease, injury to astrocytes is initiated by the action of autoantibodies targeting aquaporin 4 (AQP-4), a water channel on astrocytes.

INTRODUCTION: Loss of aquaporin 4 and glial fibrillary acidic protein (GFAP) with necrosis and demyelination is a prominent pathologic feature of neuromyelitis optica (NMO). However, the clinicopathologic significance of astrocytic damage and its relation with demyelination are unknown