{"created":"2023-07-27T06:58:43.990357+00:00","id":57703,"links":{},"metadata":{"_buckets":{"deposit":"5f98019c-d77f-46c9-9155-acdd438777d0"},"_deposit":{"created_by":18,"id":"57703","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"57703"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00057703","sets":["2812:2813:2833"]},"author_link":["2298"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2002-03-25","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"2p.","bibliographicVolumeNumber":"1999 – 2000","bibliographic_titles":[{"bibliographic_title":"平成12(2000)年度 科学研究費補助金 基盤研究(C) 研究成果報告書概要"},{"bibliographic_title":"2000 Fiscal Year Final Research Summary","bibliographic_titleLang":"en"}]}]},"item_9_creator_33":{"attribute_name":"著者別表示","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{}],"nameIdentifiers":[{},{}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"今回の研究では老人斑・神経原線維変化と神経細胞死に関する研究をおこなった。アポトーシスを示す細胞はアンギオパチーを示す小血管と古典型老人斑周囲の神経細胞とグリア細胞にみられた。神経原線維変化とアポトーシスとの関連ではタウ抗体(AT8)の免疫活性とアポトーシスとは関連がみられ、CD68やアミロイドP抗体で染色される細胞外神経原線維変化とは量的に相関が認められた。C4dやアミロイドP蛋白の免疫活性はアポトーシスの後に生じているようにみえる。Gallyas法/AT8免疫染色/TUNEL法での三重染色では、AT8陽性の神経細胞内に嗜銀性神経原線維変化が出現してくると核がTUNEL陽性となっているようである。老人斑では線維化したアミロイドの周辺に明らかなアポトーシスを示す細胞がみられ、芯のないびまん性老人斑周囲にはこれらの細胞はほとんど認められない。抗ユビキチン抗体で染色される老人斑とアポトーシス細胞の量的な相関は明確でない。統計学的には神経原線維変化よりも老人斑との相関が有意であった。またアルツハイマー病症例の非虚血性の白質変性病変では白質グリア細胞のアポトーシスが無数にみられた。グリア細胞のアポトーシスの大半は星状膠細胞と稀突起膠細胞であった。星状膠細胞は退行性変化を示すものが多く、この変化をもつ星状膠細胞にCD68陽性顆粒を胞体内に認めた。退行性変化をしめす星状膠細胞は例外なくアポトーシスを起こしており、特に側頭葉に有意に多く、白質小血管内皮細胞のアポトーシスは前頭葉と側頭葉間で差がなかった。まとめると、神経細胞とグリア細胞のアポトーシスはアミロイドベーター蛋白の沈着が深く関与しており、白質変性部位にはCD68-KP1陽性顆粒が退行性変化をもつ星状膠細胞内に認められ、同時に希突起膠細胞のアポトーシスを起こしている。今回の研究では白質変性におけるグリア細胞のアポトーシスが大きな課題として残った。","subitem_description_type":"Abstract"},{"subitem_description":"In the present study, we studied the relationship between neuronal death and occurrence of senile plaques and neurofibrillary changes. Apoptotic cells were observed in the endothelial cell of small vessels with angiopathic change and neurons and glial cells around the classic senile plaques. As for neurofibrillary changes and apoptosis, the intensity of AT8 tau immunoreactivity and the number of apoptotic cells were significantly correlated, in particular, the number of apoptotic cells significantly correlated with that of extracellular neurofibrillary tangles labeled with C4d and CD68. Immunoreactivity of C4d and amyloid P appeared to develop after apoptotic changes. Triplet labeling of Gallyas silver impregnation/ AT8 tau labeling/. TUNEL showed that occurrence of silver-stained neurofibrillary tangles in the AT8tau-positive cytoplasms contributed to the development of TUNEL-positive nuclei. Senile plaques with amyloid fibrils contained apoptotic cells around them, while the diffuse plaques contained few apoptotic cells. Quantitative correlation between density of senile plaques labeled with ubiquitin and apoptotic cells was not definite. Statistical analysis revealed that density of apoptotic cells correlated more significantly with density of senile plaques than that of neurofibrillary tangles. Non-ischemic white matter lesions in Alzheimer cases contained considerable numbers of apoptotic glial cells. They were largely astrocytes and oligodendrocytes. Many white matter astrocytes displayed regressive changes in which intracytoplasmic vacuoles were labeled with CD68. The astrocytes with regressive changes were apoptotic without exception, and these astrocytes were distributed predominantly in the temporal white matter. The density of apoptotic white matter endothelial cell was not different between temporal and frontal white matter. In summary, apoptosis of neurons and glial cells could be closely associated with beta amyloid protein deposits, CD68KP1-positive materials were found in the white matter astrocytes with regressive changes and apoptosis, and numerous oligodendrocytes were apoptotic. A role of glial apoptosis for white matter lesions in Alzheimer's diseased brains remains to be determined.","subitem_description_type":"Abstract"}]},"item_9_description_22":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究課題/領域番号:11670937, 研究期間(年度):1999 – 2000","subitem_description_type":"Other"},{"subitem_description":"出典：「アルツハイマー変化を神経細胞死に関する免疫組織学的研究」研究成果報告書　課題番号11670937\n（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） \n（ https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-11670937/116709372000kenkyu_seika_hokoku_gaiyo/）を加工して作成","subitem_description_type":"Other"}]},"item_9_description_5":{"attribute_name":"提供者所属","attribute_value_mlt":[{"subitem_description":"金沢大学医学部・附属病院","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00063973","subitem_identifier_reg_type":"JaLC"}]},"item_9_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/ja/search/?kw=50221239"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/search/?kw=50221239","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-11670937/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-11670937/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-11670937/116709372000kenkyu_seika_hokoku_gaiyo/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-11670937/116709372000kenkyu_seika_hokoku_gaiyo/","subitem_relation_type_select":"URI"}}]},"item_9_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2021-09-10"}],"displaytype":"detail","filename":"HO-PR-KOBAYASHI-K-kaken 2002-2p.pdf","filesize":[{"value":"100.9 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"HO-PR-KOBAYASHI-K-kaken 2002-2p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/57703/files/HO-PR-KOBAYASHI-K-kaken 2002-2p.pdf"},"version_id":"a90a40e2-205a-45e9-86b4-c81740a28874"}]},"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":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"アルツハイマー変化を神経細胞死に関する免疫組織学的研究","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"アルツハイマー変化を神経細胞死に関する免疫組織学的研究"},{"subitem_title":"An immunohistochemical study on Alzheimer change and neuronal death","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2833"],"pubdate":{"attribute_name":"公開日","attribute_value":"2021-09-10"},"publish_date":"2021-09-10","publish_status":"0","recid":"57703","relation_version_is_last":true,"title":["アルツハイマー変化を神経細胞死に関する免疫組織学的研究"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T14:58:24.714436+00:00"}