Neuromyelitis optica (NMO) is an autoimmune demyelinating disease characterized by the presence of anti-aquaporin-4 (AQP4) antibodies in the patient sera. We recently reported that these autoantibodies are able to bind AQP4 when organized in the supramolecular structure called the orthogonal array of particles (OAP).
Objective In neuromyelitis optica (NMO), the destruction of the blood-brain barrier (BBB) has been considered to be the first step of the disease process.
Neuromyelitis optica is an autoimmune demyelinating disease characterized by the presence of anti aquaporin-4 (AQP4) antibodies in the patient sera.
In 2004, a highly disease-specific autoantibody named NMO-IgG was discovered in patients with neuromyelitis optica (NMO) and NMO related diseases (i.e. relapsing optic neuritis and longitudinally extensive transverse myelitis). The target antigen of NMO-IgG was identified as aquaporin-4 (AQP4), the main water channel protein in the central nervous system (CNS).
We identified the autoantibody against phosphoglycerate mutase 1 (PGAM1), which is a glycolytic enzyme, in sera from multiple sclerosis (MS) patients by proteomics-based analysis. We further searched this autoantibody in sera from patients with other neurological diseases. The prevalence of the anti-PGAM1 antibody is much higher in patients with MS and neuromyelitis optica (NMO) than in those with other neurological diseases and in healthy controls.