China
Africa
Explore chapters and articles related to this topic
Diseases of the Peripheral Nerve and Mononeuropathies
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Diana Mnatsakanova, Charles K. Abrams
There is a strong association with antibodies against myelin-associated glycoprotein (anti-MAG). This is often discovered after finding an elevated IgM level on serum immunofixation electrophoresis. Patients respond poorly to immunomodulatory therapy.
Waldenström Macroglobulinemia
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Although infrequent, organ damage may result from an IgM paraprotein with autoimmune activity or altered structure prone to tissue deposition [62]. Peripheral neuropathy, seen in approximately 25%–50% of patients [63], usually present as a distal, symmetric, and slowly progressive sensorimotor neuropathy with predominantly demyelinating features in nerve conduction studies [64]. Anti-myelin–associated glycoprotein (MAG) IgM antibodies have been implicated as the cause of neuropathy in half of these patients. IgM paraprotein directed to GD1b ganglioside, sulfatide, and chondroitin sulphate have also been described, although the causal relationship is not well established [64].
The nervous system and the eye
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
James A.R. Nicoll, William Stewart, Fiona Roberts
This may occur in association with myeloma, lymphoma, and Waldenström's macroglobinaemia. In about 10% of the late-onset chronic cases there is a specific IgM antibody to myelin-associated glycoprotein. There is both axonal loss and demyelination.
Remyelination therapies for multiple sclerosis: optimizing translation from animal models into clinical trials
Published in Expert Opinion on Investigational Drugs, 2021
Rujapope Sutiwisesak, Terry C. Burns, Moses Rodriguez, Arthur E. Warrington
Pattern III and IV active lesions are characterized by profound loss of oligodendrocytes and lack of remyelination. The mode of oligodendroglial cell death is apoptosis in pattern III and non-apoptotic cell death in pattern IV. The topography of pattern IV lesions is similar to that of pattern I and II. However, pattern III lesions have an ill-defined border and demonstrate preferential loss of peri-axonal myelin-associated glycoprotein (MAG). Pattern III lesions almost always demonstrated electron microscopy (EM) based evidence of ‘dying-back oligodendrocytes’ with degeneration of the inner glial loop representing the most distal extension from the oligodendrocyte cell body [14].
Radiation-induced neuropathological changes in the oligodendrocyte lineage with relevant clinical manifestations and therapeutic strategies
Published in International Journal of Radiation Biology, 2022
Immature non-myelinating oligodendrocytes eventually develop into mature myelinating oligodendrocytes that simultaneously extend multiple fine processes that encircle and ensheath their target axons (Shimizu et al. 2018) while initiating the expression of mature oligodendrocyte or myelin-associated markers such as myelin basic protein (MBP), proteolipid protein (PLP), myelin-associated glycoprotein (MAG) (Valerio-Gomes et al. 2018), oligodendrocyte-myelin glycoprotein (OMgp) (Vourc’h et al. 2003), oligodendrocyte-specific protein (OSP) (Gow et al. 1999) and Nogo-A (Kuhlmann et al. 2007). See Figure 1 for schematic diagram.
Serum B cell activating factor (BAFF) as a biomarker for induction of remission with rituximab in ANCA-associated vasculitis
Published in Immunological Medicine, 2022
Kazuyuki Tsuboi, Kazuteru Noguchi, Masayasu Kitano, Tetsuya Furukawa, Teppei Hashimoto, Naoto Azuma, Kiyoshi Matsui
However, it has been reported that serum BAFF levels increase in patients with AAV after 1–3 months of treatment with RTX compared to pre-treatment levels [10]. Anti-myelin-associated glycoprotein (MAG) polyneuropathy is a slowly progressive distal form of mixed motor sensory polyneuropathy, and RTX has shown promise as an effective treatment. Regarding the difference in serum BAFF levels between responders and non-responders to RTX, it has been reported that serum BAFF levels in anti-MAG polyneuropathy are significantly higher in responders than in non-responders after 1 month of treatment with RTX [12].