{"created":"2023-06-19T10:54:53.352882+00:00","id":5328,"links":{},"metadata":{"_buckets":{"deposit":"9ff04a2d-7259-475d-ade5-02acb8986b40"},"_deposit":{"created_by":17,"id":"5328","owners":[17],"pid":{"revision_id":0,"type":"depid","value":"5328"},"status":"published"},"_oai":{"id":"oai:kobe-c.repo.nii.ac.jp:00005328","sets":["40:1322:1332"]},"author_link":["5860","3194"],"item_10002_biblio_info_30":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2016-12-20","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"2","bibliographicPageEnd":"140","bibliographicPageStart":"129","bibliographicVolumeNumber":"63","bibliographic_titles":[{"bibliographic_title":"神戸女学院大学論集"},{"bibliographic_title":"KOBE COLLEGE STUDIES","bibliographic_titleLang":"en"}]}]},"item_10002_description_28":{"attribute_name":"要旨(日）","attribute_value_mlt":[{"subitem_description":"加齢と共に発症する認知症は高齢化が進行する先進国に共通の社会問題となっており、中でもアルツハイマー型認知症患者の増加が問題視されている。アルツハイマー型認知症では大脳萎縮により認知機能が低下するが、その原因は老人斑として知られている大脳へのアミロイドβの沈着による神経細胞脱落と考えられている。一方、アルツハイマー型認知症の発症には性差があることも知られている。閉経前の女性は男性より発症が少なく、閉経後に男性より多く発症することより、女性ホルモンが神経細胞を保護し、閉経によりエストロゲンが低下すると、神経細胞死を顕在化させると考えられる。本研究では、女性ホルモンのエストロゲンが神経保護効果を発揮するか否かを、培養神経細胞のアミロイドβ負荷モデルを用いて検討した。神経由来株細胞PC-12にアミロイドβ凝集体（5μM）を負荷すると、LDHアッセイで定量したネクローシス、及びTUNEL法で定量したアポトーシスともに増加し、アルツハイマー型認知症におけるアミロイド蛋白による神経細胞死を模擬することができた。アミロイドβ負荷は小胞体特異的な蛍光色素を用いて測定した小胞体ストレスも増加させた。PC-12を17β-エストラジオール(0～1μM)で前処理すると、アミロイド負荷による小胞体ストレスが減少し、同時にアポトーシスによる細胞死も減少した。以上の結果より、女性ホルモンのエストロゲンは小胞体ストレスを軽減することにより細胞死を抑制し、神経保護効果を発揮することにより閉経前の女性におけるアルツハイマー型認知症を抑制している可能性が示唆される。","subitem_description_type":"Other"}]},"item_10002_description_49":{"attribute_name":"要旨（英）","attribute_value_mlt":[{"subitem_description":"Alzheimer's disease, which advances with aging, is a common social problem in developed countries experiencing a rapid increase in aged population. Amyloid β aggregates are specifically observed in cerebral cortex of Alzheimer's disease together with neuronal degeneration. Therefore, amyloid β is supposed to be the cause of cognitive disorders by inducing brain atrophy. Morbidity of Alzheimer's disease shows sex difference. Pre-menopause women have the low morbidity compared to age-matched men and the morbidity of post-menopause women surpass male counterparts, suggesting that female hormones protect neurons from degeneration. We investigated whether a female hormone, estrogen, evokes neuro-protective effects in cultured neuronal cells exposed to amyloid β to mimic Alzheimer's disease.\nRat neuronal cells (PC-12) were exposed to amyloid β aggregates (0～5μM) and two types of cell death, necrosis and apoptosis, were assessed by LDH assay and TUNEL method 24 hours after exposure, respectively. Amyloid β aggregates induced both necrosis and apoptosis dose-dependently. We also examined endoplasmic reticulum (ER) stress, which is augmented when cells process denatured proteins, with an ER specific fluorescent dye. Amyloid β aggregates also increased ER stress time-dependently compared to control cells without amyloid exposure. Pretreatment with 17β-estradiol decreased ER stress of amyloid β treated cells, which coincided with the decrease in apoptosis of the cells.\nThese results suggest that amyloid β aggregates induce neural cell death by augmenting ER stress in the cells and a female hormone,estrogen, protects neurons from degeneration by reducing ER stress. Therefore, supplementation of estrogen may decrease the morbidity of Alzheimer's disease in post-menopause women.","subitem_description_type":"Other"}]},"item_10002_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.18878/00005280","subitem_identifier_reg_type":"JaLC"}]},"item_10002_text_47":{"attribute_name":"著者所属","attribute_value_mlt":[{"subitem_text_value":"神戸女学院大学大学院人間科学研究科人間科学専攻博士前期課程"},{"subitem_text_value":"神戸女学院大学人間科学部環境・バイオサイエンス学科教授"}]},"item_10002_text_48":{"attribute_name":"雑誌書誌ID","attribute_value_mlt":[{"subitem_text_value":"AN00085725"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"山本, 智美"},{"creatorName":"ヤマモト, トモミ","creatorNameLang":"ja-Kana"},{"creatorName":"YAMAMOTO, Tomomi","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"5860","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"西田, 昌司"},{"creatorName":"ニシダ, マサシ","creatorNameLang":"ja-Kana"},{"creatorName":"NISHIDA, Masashi","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"3194","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"1000040283783","nameIdentifierScheme":"CiNii ID","nameIdentifierURI":"http://ci.nii.ac.jp/nrid/1000040283783"},{"nameIdentifier":"40283783","nameIdentifierScheme":"KAKEN-研究者検索","nameIdentifierURI":"https://nrid.nii.ac.jp/ja/nrid/1000040283783/"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-01-26"}],"displaytype":"detail","filename":"201612_177-11.pdf","filesize":[{"value":"1.2 MB"}],"format":"application/pdf","license_note":"神戸女学院大学研究所","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"201612_177-11","url":"https://kobe-c.repo.nii.ac.jp/record/5328/files/201612_177-11.pdf"},"version_id":"90b45161-f030-49ef-a828-5bb9906f98ba"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"アルツハイマー型認知症","subitem_subject_scheme":"Other"},{"subitem_subject":"アミロイドβ","subitem_subject_scheme":"Other"},{"subitem_subject":"神経細胞","subitem_subject_scheme":"Other"},{"subitem_subject":"17β-エストラジオール","subitem_subject_scheme":"Other"},{"subitem_subject":"アポトーシス","subitem_subject_scheme":"Other"},{"subitem_subject":"小胞体ストレス","subitem_subject_scheme":"Other"},{"subitem_subject":"Alzheimer's disease","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"amyloid β","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"neuron","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"17β-estradiol","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"apoptosis","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"endoplasmic reticulum stress","subitem_subject_language":"en","subitem_subject_scheme":"Other"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"departmental bulletin paper","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"女性ホルモンとアルツハイマー型認知症―アミロイドβ負荷による神経細胞障害に対する17β-エストラジオールの保護効果―","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"女性ホルモンとアルツハイマー型認知症―アミロイドβ負荷による神経細胞障害に対する17β-エストラジオールの保護効果―"},{"subitem_title":"Female Hormones and Alzheimer's Disease ー The Protective Effect of 17β-Estradiol Against Neural Cell Injuries Caused by the Exposure to Amyloid β ー","subitem_title_language":"en"}]},"item_type_id":"10002","owner":"17","path":["1332"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-01-26"},"publish_date":"2017-01-26","publish_status":"0","recid":"5328","relation_version_is_last":true,"title":["女性ホルモンとアルツハイマー型認知症―アミロイドβ負荷による神経細胞障害に対する17β-エストラジオールの保護効果―"],"weko_creator_id":"17","weko_shared_id":-1},"updated":"2023-06-19T11:32:59.421960+00:00"}