The decline of the expression of low density lipoprotein receptor-related protein 1 (LRP1) during normal ageing and in Alzheimer's disease
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DOI[10.24659/gsr.9.2_42]のデータに遷移します
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- 資料種別
- 記事
- 著者・編者
- Nikola Barić
- 出版事項
- 出版年月日等
- 2022-06-30
- 出版年（W3CDTF）
- 2022-06-30
- タイトル（掲載誌）
- Glycative stress research
- 巻号年月日等（掲載誌）
- 9(2)
- 掲載巻
- 9(2)
- ISSN（掲載誌）
- 2188-3610
- ISSN-L（掲載誌）
- 2188-3610
- 本文の言語コード
- eng
- DOI
- 10.24659/gsr.9.2_42
- 国立国会図書館永続的識別子
- info:ndljp/pid/13120769
- コレクション（共通）
- コレクション（障害者向け資料：レベル1）
- 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
- 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（国立国会図書館永続的識別子）
- info:ndljp/pid/13120767
- 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
- 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
- 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（国立国会図書館永続的識別子）
- info:ndljp/pid/13120769
- 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
- 書誌ID（NDLBibID）
- 032834788
- 整理区分コード
- 632
- 要約等
- Considering the importance of the low-density lipoprotein receptor-related protein 1 (LRP1) as the scavenger of harmful waste products from the brain, especially amyloid beta (Aβ), and as the mediator in a number of signal events, LRP1 is increasingly becoming the object of intensive researches. Alzheimer's disease (AD), as proved, is the result of the disordered Aβ intracerebral homeostasis, characterized by intensive Aβ accumulation in the brain, induced primarily by the Aβ disordered efflux from the brain, and not by its increased production. This elevated Aβ accumulation in the brain structures leads to the increase of the local oxidative stress with intensively harmful effects of the generated free radicals, especially hydroxyl radicals (*OHs). This condition is accompanied by severe oxidative damages of a number of vital brain structures, especially endothelial cell membranes. LRP1, at the level of blood-brain barrier (BBB) endothelial cells, initiated by Aβ binding to its ligand binding domains, especially domains II and IV, induces specific conformational changes in both receptor domains, which causes the onset of pulling forces that, starting from the point of Aβ binding to LRP1, spread along the receptor structure in both directions. Especially important is the spreading of these forces towards the abluminal membrane, their passing across this membrane and entering the receptor tail region and the compound structure of its molecules. The activation of these molecular systems leads to endocytosis, transcytosis, and exocytosis of Aβ bound to the receptor, into the capillary blood of the BBB. The drained Aβ travels further on by the blood stream, exits from the brain, and arrives at the positions of its degradation and elimination, liver, kidneys, spleen, and skin. Investigations have shown that generally, the expression of LRP1 in the BBB endothelial cell system declines during normal ageing, and especially in AD. It is evident that this phenomenon weakens the Aβ drainage from the brain. The actual question is what causes the LRP1 expression drop in these conditions, and if it is possible to slow down this drop. In this respect, this review paper intends to explain the problem of the LRP1 expression decline, and its possible increase, i.e., the retardation of the AD pathophysiological course.
- DOI
- 10.24659/gsr.9.2_42
- 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
- 要約等
- Considering the importance of the low-density lipoprotein receptor-related protein 1 (LRP1) as the scavenger of harmful waste products from the brain, especially amyloid beta (Aβ), and as the mediator in a number of signal events, LRP1 is increasingly becoming the object of intensive researches. Alzheimer's disease (AD), as proved, is the result of the disordered Aβ intracerebral homeostasis, characterized by intensive Aβ accumulation in the brain, induced primarily by the Aβ disordered efflux from the brain, and not by its increased production. This elevated Aβ accumulation in the brain structures leads to the increase of the local oxidative stress with intensively harmful effects of the generated free radicals, especially hydroxyl radicals (*OHs). This condition is accompanied by severe oxidative damages of a number of vital brain structures, especially endothelial cell membranes. LRP1, at the level of blood-brain barrier (BBB) endothelial cells, initiated by Aβ binding to its ligand binding domains, especially domains II and IV, induces specific conformational changes in both receptor domains, which causes the onset of pulling forces that, starting from the point of Aβ binding to LRP1, spread along the receptor structure in both directions. Especially important is the spreading of these forces towards the abluminal membrane, their passing across this membrane and entering the receptor tail region and the compound structure of its molecules. The activation of these molecular systems leads to endocytosis, transcytosis, and exocytosis of Aβ bound to the receptor, into the capillary blood of the BBB. The drained Aβ travels further on by the blood stream, exits from the brain, and arrives at the positions of its degradation and elimination, liver, kidneys, spleen, and skin. Investigations have shown that generally, the expression of LRP1 in the BBB endothelial cell system declines during normal ageing, and especially in AD. It is evident that this phenomenon weakens the Aβ drainage from the brain. The actual question is what causes the LRP1 expression drop in these conditions, and if it is possible to slow down this drop. In this respect, this review paper intends to explain the problem of the LRP1 expression decline, and its possible increase, i.e., the retardation of the AD pathophysiological course.
- DOI
- 10.24659/gsr.9.2_42
- 関連情報（URI）
- 連携機関・データベース
- 国立情報学研究所 : CiNii Research
- 提供元機関・データベース
- 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
- 書誌ID（NDLBibID）
- 03283478813120769