Proteomic analysis of the cerebrospinal fluid in multiple sclerosis and neuromyelitis optica patients Authors: Shoufeng Jiang, Jiong Wu, Yi Yang, Jianren Liu, Yao Ding, Meiping Ding Affiliations: Department of Neurology, the Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, P.R.
Impaired regulatory function and enhanced intrathecal activation of B cells in neuromyelitis optica: distinct from multiple sclerosis. Quan C, Yu H, Qiao J, Xiao B, Zhao G, Wu Z, Li Z, Lu C. Source Department of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China
Takeshi Matsuoka 1,2 , Satoshi O.
Aquaporin-4 (AQP4) exists as two major isoforms that differ in the length of the N terminus, the shorter AQP4-M23 and the longer AQP4-M1. Both isoforms form tetramers, which can further aggregate in the plasma membrane to form typical orthogonal arrays of particles (OAPs) whose dimension depends on the ratio of the M1 and M23. In this study, we tested the hypothesis that the M23 isoform can be produced directly by the M1 mRNA
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 In neuromyelitis optica (NMO), the destruction of the blood-brain barrier (BBB) has been considered to be the first step of the disease process.
PURPOSE: To better understand the pathophysiological mechanisms underlying neuromyelitis optica (NMO), we developed a proteomics platform for biomarker discovery in the cerebrospinal fluid (CSF) of patients with NMO.
There is a complex, diverse array of “preceding environmental events” and perhaps unconnected immune-related events which are often associated with the period before patients are diagnosed with NMO. In this review we discuss in detail how the different isoform structures of AQP4 in different membrane locales and in different cell types might be related to pathology. Changes in AQP4 expression in CNS and non-CNS tissue can be regulated by inflammatory mediators induced during and following infection or by underlying autoimmunity and can result in the induction of AQP4-specific lymphocytes and ensuing pathogenesis.