The decline of the expression of low density lipoprotein receptor-related protein 1 (LRP1) during normal ageing and in Alzheimer's disease

• Material Type: 記事
• Title: The decline of the expression of low density lipoprotein receptor-related protein 1 (LRP1) during normal ageing and in Alzheimer's disease
• Author/Editor: Nikola Barić
• Publication, Distribution, etc.: 日本 : 糖化ストレス研究会
• Publication Date: 2022-06-30
• Publication Date (W3CDTF): 2022-06-30
• Periodical title: Glycative stress research
• No. or year of volume/issue: 9(2)
• Volume: 9(2)
• ISSN (Periodical Title): 2188-3610
• ISSN-L (Periodical Title): 2188-3610
• Text Language Code: eng
• DOI: 10.24659/gsr.9.2_42; https://doi.org/10.24659/gsr.9.2_42
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• 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
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• Related Material (URI): https://dl.ndl.go.jp/info:ndljp/pid/13120769
• Related Material (Persistent ID (NDL)): info:ndljp/pid/13120769; https://dl.ndl.go.jp/info:ndljp/pid/13120769
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• Bibliographic ID (NDL): 032834788; http://id.ndl.go.jp/bib/032834788
• Bibliographic Record Category (NDL): 632

• Summary, etc.: 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
• Access Restrictions: インターネット公開
• Data Provider (Database): 科学技術振興機構 : J-STAGE; http://www.jstage.jst.go.jp

• Summary, etc.: 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; https://doi.org/10.24659/gsr.9.2_42
• Related Material (URI): http://id.ndl.go.jp/bib/032834788; https://ndlsearch.ndl.go.jp/books/R000000004-I032834788; https://dl.ndl.go.jp/pid/13120769; http://id.ndl.go.jp/digimeta/13120769; https://search.jamas.or.jp/link/ui/2023252495
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• Bibliographic ID (NDL): 032834788; http://id.ndl.go.jp/bib/032834788; 13120769; http://id.ndl.go.jp/bib/13120769