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Acetylcholine receptors loss and postsynaptic damage in MuSK antibody–positive myasthenia gravis
Author(s) -
Shiraishi Hirokazu,
Motomura Masakatsu,
Yoshimura Toshiro,
Fukudome Takayasu,
Fukuda Taku,
Nakao Yoko,
Tsujihata Mitsuhiro,
Vincent Angela,
Eguchi Katsumi
Publication year - 2005
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.20341
Subject(s) - myasthenia gravis , acetylcholine receptor , antibody , postsynaptic potential , receptor , acetylcholine , neuromuscular junction , endocrinology , chemistry , medicine , immunology , biology , neuroscience
Muscle‐specific tyrosine kinase (MuSK) antibodies are found in some patients with “seronegative” myasthenia gravis (MG), but how they cause myasthenic symptoms is not clear. We visualized acetylcholine receptors (AChRs) and complement component 3 (C3) in muscle biopsies from 10 Japanese MG patients with MuSK antibodies, compared with 42 with AChR antibodies. The AChR density was not significantly decreased in MuSK antibody (Ab)–positive end‐plates compared with AChR antibody–positive end‐plates, and C3 was detected in only two of eight MuSK Ab–positive patients. MuSK antibodies do not appear to cause substantial AChR loss, complement deposition, or morphological damage. Effects on MuSK function need to be explored. Ann Neurol 2005;57:289–293