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  1. 0 資料タイプ別
  2. 03 紀要論文
  1. 250 大学院医歯学総合研究科(医)
  2. 20 紀要
  3. 02 新潟医学会雑誌
  4. 第113巻第10号

1) 痴呆の分子機構(シンポジウム 「痴呆の病態と治療 : 分子生物学から地域医療までの統合」, 第545回新潟医学会)

http://hdl.handle.net/10191/46891
http://hdl.handle.net/10191/46891
f5901c1a-4295-47b7-b4b5-544d0bee14d8
名前 / ファイル ライセンス アクション
113(10)_443-450.pdf 113(10)_443-450.pdf (1.4 MB)
Item type 紀要論文 / Departmental Bulletin Paper(1)
公開日 2017-02-28
タイトル
タイトル 1) 痴呆の分子機構(シンポジウム 「痴呆の病態と治療 : 分子生物学から地域医療までの統合」, 第545回新潟医学会)
タイトル
言語 en
タイトル 1) 痴呆の分子機構(シンポジウム 「痴呆の病態と治療 : 分子生物学から地域医療までの統合」, 第545回新潟医学会)
言語
言語 jpn
キーワード
主題Scheme Other
主題 Alzheimer disease
キーワード
主題Scheme Other
主題 genetic heterogenicity
キーワード
主題Scheme Other
主題 amyloid precursor protein gene
キーワード
主題Scheme Other
主題 presenilin gene
キーワード
主題Scheme Other
主題 apolipoprotein E gene
キーワード
主題Scheme Other
主題 アルツハイマー病
キーワード
主題Scheme Other
主題 アミロイド前駆体蛋白遺伝子
キーワード
主題Scheme Other
主題 プレセニリン遺伝子
キーワード
主題Scheme Other
主題 アポリポ蛋白E遺伝子
資源タイプ
資源 http://purl.org/coar/resource_type/c_6501
タイプ departmental bulletin paper
その他のタイトル
その他のタイトル Molecular Mechanisms of Dementia
著者 奥泉, 薫

× 奥泉, 薫

WEKO 101374

奥泉, 薫

Search repository
辻, 省次

× 辻, 省次

WEKO 101375

辻, 省次

Search repository
著者別名
識別子 101376
識別子Scheme WEKO
姓名 Okuizumi, Kaoru
著者別名
識別子 101377
識別子Scheme WEKO
姓名 Tsuji, Shoji
抄録
内容記述タイプ Abstract
内容記述 Advances in molecular genetic approaches have provided new insights into the pathogenesis of various neurodegenerative disorders with dementia. Alzheimer disease (AD) is by far the most common cause of dementia in human. Recent molecular genetic analyses have revealed that AD is etiologically heterogeneous. Early-onset familial AD has been demonstrated to be induced by mutations of the causative genes including amyloid precursor protein gene (APP), presenilin-1 (PS-1) and presenilin-2 (PS-2) genes. Initially, missense mutations of the gene encoding the amyloid precursor protein were identified as the causative mutations for AD. Subsequently, mutations of presenilin-1 and presenili-2 gene have been identified in a number of pedigrees with early-onset familial AD. Although these mutations have been found to be causative for familial forms of AD (FAD), the majority of AD occures as sporadic cases. Sporadic AD is demonstrated to be a polygenic disorder caused by several genetic risk factors. APOE 4, one of the alleles of the apolipoprotein E gene, has been established as being a major risk factor for sporadic and late-onset familial AD. Other risk factors are currently under investigation. The above mentioned studies strongly suggest the involvement of several key molecules in the pathogenesis of AD. Furthermore, it is strongly expected that preventive measures or new treatment methods for AD based on the genetic risk factors will be developed.
書誌情報 新潟医学会雑誌
en : 新潟医学会雑誌

巻 113, 号 10, p. 443-450, 発行日 1999-10
出版者
出版者 新潟医学会
ISSN
収録物識別子タイプ ISSN
収録物識別子 00290440
書誌レコードID
収録物識別子タイプ NCID
収録物識別子 AN00182415
著者版フラグ
値 publisher
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