Amyloid beta clearance and microglia : effects of glycative stress and melatonin

• 資料種別: 記事
• タイトル: Amyloid beta clearance and microglia : effects of glycative stress and melatonin
• 著者・編者: Yoshikazu Yonei; Toshio Taira; Shino Otaka
• 出版事項: 日本 : 糖化ストレス研究会
• 出版年月日等: 2022-09-30
• 出版年（W3CDTF）: 2022-09-30
• 並列タイトル等: アミロイドβクリアランスとミクログリア : 糖化ストレスおよびメラトニンの影響
• タイトル（掲載誌）: Glycative stress research
• 巻号年月日等（掲載誌）: 9(3)
• 掲載巻: 9(3)
• ISSN（掲載誌）: 2188-3610
• ISSN-L（掲載誌）: 2188-3610
• 本文の言語コード: eng; jpn
• DOI: 10.24659/gsr.9.3_135; https://doi.org/10.24659/gsr.9.3_135
• 国立国会図書館永続的識別子: info:ndljp/pid/13120781; https://dl.ndl.go.jp/pid/13120781
• コレクション（共通）: 障害者向け資料
• コレクション（障害者向け資料：レベル1）: テキストデータ
• コレクション（個別）: 国立国会図書館デジタルコレクション > 電子書籍・電子雑誌 > その他; https://dl.ndl.go.jp/collections/B00035
• 収集根拠: オンライン資料収集制度
• 受理日（W3CDTF）: 2023-12-08T11:19:22+09:00
• 保存日（W3CDTF）: 2023-05-20
• 記録形式（IMT）: application/pdf
• オンライン閲覧公開範囲: 国立国会図書館内限定公開
• デジタル化資料送信: 図書館・個人送信対象外
• 遠隔複写可否（NDL）: 可
• 掲載誌（URI）: https://www.toukastress.jp/webj/page-1
• 掲載誌（国立国会図書館永続的識別子）: info:ndljp/pid/13120776; https://dl.ndl.go.jp/pid/13120776
• 連携機関・データベース: 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

• コレクション（個別）: 国立国会図書館デジタルコレクション > 電子書籍・電子雑誌 > その他; https://dl.ndl.go.jp/collections/B00035
• オンライン閲覧公開範囲: 国立国会図書館内限定公開
• デジタル化資料送信: 図書館・個人送信対象外
• 遠隔複写可否（NDL）: 可
• 所蔵機関: 国立国会図書館
• 請求記号: Z63-D541
• 関連情報（URI）: https://dl.ndl.go.jp/info:ndljp/pid/13120781
• 関連情報（国立国会図書館永続的識別子）: info:ndljp/pid/13120781; https://dl.ndl.go.jp/info:ndljp/pid/13120781
• 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）: 032834806; http://id.ndl.go.jp/bib/032834806
• 整理区分コード: 632

• 要約等: The physiological role of amyloid-β (Aβ) is unknown, while it plays an important role in the onset and progression of Alzheimer's disease (AD). Aβ polymerization leads to enhanced neurotoxicity, persistent degradation, and deposition in the brain, resulting in decreased Aβ clearance. Diabetes mellitus and poor sleep quality are representative risk factors for the development of AD. Methylglyoxal (MGO) and acrolein are increased in diabetic patients, a representative disease with high glycative stress, and melatonin secretion is decreased during poor sleep quality. In this study, we focused on the Aβ phagocytosis of microglia, which plays a role in Aβ clearance, and examined the effects of Aβ glycation and melatonin. Glycated Aβ was prepared by MGO or acrolein treatment. Fluorescently labeled TAMRA-Aβ and primary rat microglial cells (Cosmo Bio) were used in the experiments. Several new findings were obtained from this experiment. First, microglia phagocytose Aβ, while their phagocytic capacity for glycated Aβ was markedly reduced. Second, Aβ phagocytosis was enhanced by melatonin. Concurrently, spontaneous death of cultured microglia was greater when Aβ was not added than when Aβ was. These findings suggest that prevention of Aβ glycation by countermeasures against glycative stress and prevention of AD progression by lifestyle, <i>i.e.</i>, improvement of sleep quality, are important, rather than elimination of Aβ as has been conventionally practiced.
• DOI: 10.24659/gsr.9.3_135
• 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: The physiological role of amyloid-β (Aβ) is unknown, while it plays an important role in the onset and progression of Alzheimer's disease (AD). Aβ polymerization leads to enhanced neurotoxicity, persistent degradation, and deposition in the brain, resulting in decreased Aβ clearance. Diabetes mellitus and poor sleep quality are representative risk factors for the development of AD. Methylglyoxal (MGO) and acrolein are increased in diabetic patients, a representative disease with high glycative stress, and melatonin secretion is decreased during poor sleep quality. In this study, we focused on the Aβ phagocytosis of microglia, which plays a role in Aβ clearance, and examined the effects of Aβ glycation and melatonin. Glycated Aβ was prepared by MGO or acrolein treatment. Fluorescently labeled TAMRA-Aβ and primary rat microglial cells (Cosmo Bio) were used in the experiments. Several new findings were obtained from this experiment. First, microglia phagocytose Aβ, while their phagocytic capacity for glycated Aβ was markedly reduced. Second, Aβ phagocytosis was enhanced by melatonin. Concurrently, spontaneous death of cultured microglia was greater when Aβ was not added than when Aβ was. These findings suggest that prevention of Aβ glycation by countermeasures against glycative stress and prevention of AD progression by lifestyle, <i>i.e.</i>, improvement of sleep quality, are important, rather than elimination of Aβ as has been conventionally practiced.
• DOI: 10.24659/gsr.9.3_135; https://doi.org/10.24659/gsr.9.3_135
• 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/032834806; https://ndlsearch.ndl.go.jp/books/R000000004-I032834806; https://dl.ndl.go.jp/pid/13120781; http://id.ndl.go.jp/digimeta/13120781; https://search.jamas.or.jp/link/ui/2023284390
• 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; 科学研究費助成事業データベース; https://kaken.nii.ac.jp/ja
• 書誌ID（NDLBibID）: 032834806; http://id.ndl.go.jp/bib/032834806; 13120781; http://id.ndl.go.jp/bib/13120781