Amyloid beta clearance and microglia : effects of glycative stress and melatonin
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DOI[10.24659/gsr.9.3_135]to the data of the same series
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- Material Type
- 記事
- Author/Editor
- Yoshikazu YoneiToshio TairaShino Otaka
- Publication, Distribution, etc.
- Publication Date
- 2022-09-30
- Publication Date (W3CDTF)
- 2022-09-30
- Alternative Title
- 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
- Periodical title
- Glycative stress research
- No. or year of volume/issue
- 9(3)
- Volume
- 9(3)
- ISSN (Periodical Title)
- 2188-3610
- ISSN-L (Periodical Title)
- 2188-3610
- Text Language Code
- engjpn
- DOI
- 10.24659/gsr.9.3_135
- Persistent ID (NDL)
- info:ndljp/pid/13120781
- Collection
- Collection (Materials For Handicapped People:1)
- Collection (particular)
- 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
- Acquisition Basis
- オンライン資料収集制度
- Date Accepted (W3CDTF)
- 2023-12-08T11:19:22+09:00
- Date Captured (W3CDTF)
- 2023-05-20
- Format (IMT)
- application/pdf
- Access Restrictions
- 国立国会図書館内限定公開
- Service for the Digitized Contents Transmission Service
- 図書館・個人送信対象外
- Availability of remote photoduplication service
- 可
- Periodical Title (URI)
- Periodical Title (Persistent ID (NDL))
- info:ndljp/pid/13120776
- Data Provider (Database)
- 国立国会図書館 : 国立国会図書館デジタルコレクション
- Collection (particular)
- 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
- Access Restrictions
- 国立国会図書館内限定公開
- Service for the Digitized Contents Transmission Service
- 図書館・個人送信対象外
- Availability of remote photoduplication service
- 可
- Holding library
- 国立国会図書館
- Call No.
- Z63-D541
- Related Material (URI)
- Related Material (Persistent ID (NDL))
- info:ndljp/pid/13120781
- Data Provider (Database)
- 国立国会図書館 : 国立国会図書館雑誌記事索引
- Bibliographic ID (NDL)
- 032834806
- Bibliographic Record Category (NDL)
- 632
- Summary, etc.
- 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
- Access Restrictions
- インターネット公開
- Data Provider (Database)
- 科学技術振興機構 : J-STAGE
- Summary, etc.
- 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
- Access Restrictions
- インターネット公開
- Related Material (URI)
- Data Provider (Database)
- 国立情報学研究所 : CiNii Research
- Original Data Provider (Database)
- Japan Link Center雑誌記事索引データベース雑誌記事索引データベース科学研究費助成事業データベース科学研究費助成事業データベース
- Bibliographic ID (NDL)
- 03283480613120781