書誌事項
- タイトル別名
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- Effects of nicotinic acetylcholine receptors on neurons, microglia, and bone marrow-derived microglia-like cells for the treatment of Alzheimer's disease.
抄録
<p>The accumulation of amyloid-β peptides (Aβ) is a critical trigger of Alzheimer's disease (AD) pathogenesis. Aβ is derived from sequential proteolysis of amyloid precursor protein by β- and γ-secretases. Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels. Microglia and bone marrow-derived microglia-like (BMDML) cells have Aβ phagocytic function, and nicotinic stimulation promotes microglial Aβ phagocytosis. However, it is not yet known the nicotinic effects on BMDML cells and nAChR subtypes which involve in the promotion of microglial Aβ phagocytosis. We here found that the stimulation of nAChRs promoted Aβ phagocytosis in BMDML cells and α7 nAChR was involved in the promotion of microglial Aβ phagocytosis. In a mouse model of AD, stimulation of α7 nAChR attenuated brain Aβ burden and memory dysfunction. Moreover, α7 nAChR agonist suppressed γ-secretase activity. Results suggests that α7 nAChR subtype is a reasonable drug discovery target in AD, and the stimulation of nAChRs in BMDML cells may be a beneficial option for the development of the cell therapy in AD.</p>
収録刊行物
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- 日本薬理学会年会要旨集
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日本薬理学会年会要旨集 92 (0), 1-P-010-, 2019
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390565134837312768
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- NII論文ID
- 130007812573
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- ISSN
- 24354953
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可