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We previously reported anti\u2010aquaporin\u20104 (anti\u2010\n AQP4<\/jats:styled-content>\n ) antibody\u2010dependent\n AQP4<\/jats:styled-content>\n loss occurs in some\n NMO<\/jats:styled-content>\n patients, while antibody\u2010independent\n AQP4<\/jats:styled-content>\n astrocytopathy can occur in heterogeneous demyelinating conditions, including\n MS<\/jats:styled-content>\n ,\n NMO<\/jats:styled-content>\n and\n BD<\/jats:styled-content>\n . To investigate the relationship between astrocytopathy and demyelination, we focused on connexins (\n Cxs<\/jats:styled-content>\n ), which form gap junctions (\n GJs<\/jats:styled-content>\n ) between astrocytes and oligodendrocytes and maintain homeostasis in the\n CNS<\/jats:styled-content>\n . We evaluated expression of astrocytic\n Cx43<\/jats:styled-content>\n \/\n Cx30<\/jats:styled-content>\n and oligodendrocytic\n Cx47<\/jats:styled-content>\n \/\n Cx32<\/jats:styled-content>\n in autopsied materials from\n MS<\/jats:styled-content>\n ,\n NMO<\/jats:styled-content>\n and\n BD<\/jats:styled-content>\n patients. Astrocytic\n Cx43<\/jats:styled-content>\n and oligodendrocytic\n Cx32<\/jats:styled-content>\n \/\n Cx47<\/jats:styled-content>\n expressions were significantly diminished in both demyelinated and preserved myelin layers in all\n BD<\/jats:styled-content>\n samples. In the leading edge of\n BD<\/jats:styled-content>\n lesions,\n Cx43<\/jats:styled-content>\n and\n AQP4<\/jats:styled-content>\n loss preceded\n Cx32<\/jats:styled-content>\n \/\n Cx47<\/jats:styled-content>\n loss. Half of the\n NMO<\/jats:styled-content>\n and\n MS<\/jats:styled-content>\n samples showed preferential loss of astrocytic\n Cx43<\/jats:styled-content>\n expression in actively demyelinating and chronic active lesions, where heterotypic\n Cx43<\/jats:styled-content>\n \/\n Cx47<\/jats:styled-content>\n astrocyte\u2010oligodendrocyte\n GJs<\/jats:styled-content>\n were lost. Cases with\n Cx43<\/jats:styled-content>\n loss were significantly associated with rapid disease progression, regardless of the disease phenotype. Pathologically,\n Cx43<\/jats:styled-content>\n loss was frequently accompanied by distal oligodendrogliopathy. Our findings suggest that\n Cx43<\/jats:styled-content>\n astrocytopathy can occur in\n MS<\/jats:styled-content>\n ,\n BD<\/jats:styled-content>\n and\n NMO<\/jats:styled-content>\n . Moreover, astrocytic\n Cx43<\/jats:styled-content>\n loss may be associated with disease aggressiveness and distal oligodendrogliopathy in demyelinating conditions. Early disruption of glial communications via\n GJs<\/jats:styled-content>\n may cause loss of glia syncytium, thereby inducing oligodendroglial damage and myelin loss. Inhibition of\n C<\/jats:styled-content>\n x hemichannels and restoration of\n GJs<\/jats:styled-content>\n may be a possible therapeutic target for demyelinating disorders.\n <\/jats:p>","DOI":"10.1111\/neup.12211","type":"journal-article","created":{"date-parts":[[2015,5,28]],"date-time":"2015-05-28T09:47:14Z","timestamp":1432806434000},"page":"469-480","source":"Crossref","is-referenced-by-count":61,"title":["Early disruption of glial communication via connexin gap junction in multiple sclerosis,\n B<\/scp>\n al\u00f3's disease and neuromyelitis optica"],"prefix":"10.1111","volume":"35","author":[{"given":"Katsuhisa","family":"Masaki","sequence":"first","affiliation":[{"name":"Department of Neurology Neurological Institute Graduate School of Medical Sciences Kyushu University Fukuoka 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