免疫関連性ニューロパチー(第49回日本神経学会総会(2008年) ; シンポジウム 末梢神経障害の研究--最近の進歩)

• 資料種別: 記事
• タイトル: 免疫関連性ニューロパチー
• 著者・編者: 楠 進
• シリーズタイトル: 第49回日本神経学会総会(2008年) ; シンポジウム 末梢神経障害の研究--最近の進歩
• 著者標目: 楠 進
• 並列タイトル等: Immune-mediated neuropathy
• タイトル（掲載誌）: 臨床神経学 = Clinical neurology / 日本神経学会 編
• 巻号年月日等（掲載誌）: 48(11) 2008.11
• 掲載巻: 48
• 掲載号: 11
• 掲載ページ: 1023～1025
• 掲載年月日（W3CDTF）: 2008-11
• ISSN（掲載誌）: 0009-918X
• ISSN-L（掲載誌）: 0009-918X
• 出版事項（掲載誌）: 東京 : 日本神経学会
• 出版地（国名コード）: JP
• 本文の言語コード: jpn
• 件名標目: ギランバレー症候群; 脱髄性ニューロパチー; 軸索障害性ニューロパチー; 抗ガングリオシド抗体; ガングリオシド複合体; Guillain-Barre syndrome; demyelinating neuropathy; axonal neuropathy; antiganglioside antibody; ganglioside complex
• NDLC: ZS31
• 対象利用者: 一般
• 所蔵機関: 国立国会図書館
• 請求記号: Z19-298
• 連携機関・データベース: 国立国会図書館 : 国立国会図書館雑誌記事索引; https://ndlsearch.ndl.go.jp
• 書誌ID（NDLBibID）: 9758131; http://id.ndl.go.jp/bib/9758131
• 整理区分コード: 632

• 要約等: Guillain-Barré syndrome (GBS) has two types; acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). Recently, a nation-wide retrospective study showed that the rate of AMAN is higher in Japan than in western countries. A prospective study is now in progress. Elevated titers of serum anti-ganglioside antibodies are characteristic of GBS. Complement system has been shown to be involved in the anti-ganglioside antibody-mediated pathogenetic mechanisms. Some GBS patients have antibodies specific to a conformational epitope formed by two different gangliosides. Among such anti-ganglioside complex antibodies, anti-GD1a/GD1b IgG antibodies are shown to be associated with severe GBS requiring artificial ventilation. In contrast, antibodies highly specific to GD1b are associated with GBS with ataxia. Sensory ataxic neuropathy is induced by sensitization of rabbits with GD1b. An apoptotic mechanism has recently been shown to be involved in the pathogenesis of this animal model. Most of the patients with Fisher syndrome have anti-GQ1b IgG antibodies. Recent investigation on anti-ganglioside complex antibody showed that antibodies in Fisher syndrome can be subdivided into the three groups; GQ1b-specific, GQ1b/GM1-specific, and GQ1b/GD1a-specific. Research on antibodies to gangliosides and ganglioside complexes will provide us with a clue to develop a novel treatment of GBS.<br>
• DOI: 10.5692/clinicalneurol.48.1023
• オンライン閲覧公開範囲: インターネット公開
• 連携機関・データベース: 科学技術振興機構 : J-STAGE; http://www.jstage.jst.go.jp

• 要約等: Guillain-Barré syndrome (GBS) has two types; acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). Recently, a nation-wide retrospective study showed that the rate of AMAN is higher in Japan than in western countries. A prospective study is now in progress. Elevated titers of serum anti-ganglioside antibodies are characteristic of GBS. Complement system has been shown to be involved in the anti-ganglioside antibody-mediated pathogenetic mechanisms. Some GBS patients have antibodies specific to a conformational epitope formed by two different gangliosides. Among such anti-ganglioside complex antibodies, anti-GD1a/GD1b IgG antibodies are shown to be associated with severe GBS requiring artificial ventilation. In contrast, antibodies highly specific to GD1b are associated with GBS with ataxia. Sensory ataxic neuropathy is induced by sensitization of rabbits with GD1b. An apoptotic mechanism has recently been shown to be involved in the pathogenesis of this animal model. Most of the patients with Fisher syndrome have anti-GQ1b IgG antibodies. Recent investigation on anti-ganglioside complex antibody showed that antibodies in Fisher syndrome can be subdivided into the three groups; GQ1b-specific, GQ1b/GM1-specific, and GQ1b/GD1a-specific. Research on antibodies to gangliosides and ganglioside complexes will provide us with a clue to develop a novel treatment of GBS.<br>
• DOI: 10.5692/clinicalneurol.48.1023; https://doi.org/10.5692/clinicalneurol.48.1023
• オンライン閲覧公開範囲: インターネット公開
• 関連情報（URI）: http://id.ndl.go.jp/bib/9758131; https://ndlsearch.ndl.go.jp/books/R000000004-I9758131; https://search.jamas.or.jp/link/ui/2009111514
• 参照: Anti-ganglioside complex antibodies associated with severe disability in GBS; https://cir.nii.ac.jp/crid/1360292619317616128; GD1b-specific antibody induces ataxia in Guillain-Barré syndrome; https://cir.nii.ac.jp/crid/1360292619681081472; Anti-GM1 Antibodies Cause Complement-Mediated Disruption of Sodium Channel Clusters in Peripheral Motor Nerve Fibers; https://cir.nii.ac.jp/crid/1360855568849725184; Electrophysiological classification of guillain‐barré syndrome: Clinical associations and outcome; https://cir.nii.ac.jp/crid/1360855569143759744; Apoptosis of primary sensory neurons in GD1b-induced sensory ataxic neuropathy; https://cir.nii.ac.jp/crid/1360855571312853120; Eculizumab prevents anti-ganglioside antibody-mediated neuropathy in a murine model; https://cir.nii.ac.jp/crid/1361981470600918912; Anti-ganglioside complex antibodies in Miller Fisher syndrome; https://cir.nii.ac.jp/crid/1363107371386537344; Ganglioside complexes as new target antigens in Guillain–Barré syndrome; https://cir.nii.ac.jp/crid/1363670318352082816; Anti-ganglioside antibody-mediated neuronal cytotoxicity and its protection by intravenous immunoglobulin: implications for immune neuropathies; https://cir.nii.ac.jp/crid/1363670318879533568
• 連携機関・データベース: 国立情報学研究所 : CiNii Research; https://cir.nii.ac.jp/
• 提供元機関・データベース: Japan Link Center; https://japanlinkcenter.org/top; 雑誌記事索引データベース; https://ndlsearch.ndl.go.jp; Crossref; https://www.crossref.org; CiNii Articles
• 書誌ID（NDLBibID）: 9758131; http://id.ndl.go.jp/bib/9758131
• NII論文ID: 10024898855