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）

フォーマット:

論文(リポジトリ)

責任表示:

奥泉, 薫 ; 辻, 省次

出版情報:

新潟医学会, 1999-10

掲載情報:

新潟医学会雑誌 — 新潟医学会雑誌

ISSN:

00290440      

著者名:

• 奥泉, 薫
• 辻, 省次

巻:

113

通号:

10

開始ページ:

443

終了ページ:

450

概要:

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. 続きを見る

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