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  会員専用

• ホーム
• 51巻11号
• 臨床神経, 51：979−981, 2011
• 51巻11号目次

＜シンポジウム14―2＞神経変性をどう考えるか？病態理解に至る最近の進歩

DNA損傷修復からみた神経変性機序

岡澤　均

東京医科歯科大学難治疾患研究所神経病理学分野〔〒113―8510 東京都文京区湯島1―5―45〕

Nuclear dysfunctions have been implicated in the pathology of polyglutamine diseases, while the details remain unclear. By employing various omics approaches, we have identified target molecules of mutant polyglutamine proteins in the nucleus. Proteome analysis of soluble nuclear proteins identified decreased HMGB1/2 in vulnerable neurons of Huntington's disease (HD) and spinocerebellar ataxia type 1 (SCA1). Interactome analysis unraveled Ku70 as a direct binding partner of mutant huntingtin. DNA damage repair is significantly impaired by interaction of mutant polyglutamine proteins with HMGB or Ku70, and the functional rescue of these molecules alleviated symptoms and pathologies of HD and SCA1. These results strongly suggest that impairment of DNA damage repair is a common pathology shared by multiple polyglutamine diseases.
Full Text of this Article in Japanese PDF (337K)

(臨床神経, 51：979−981, 2011)
key words：ポリグルタミン病，DNA修復，DNA損傷，分子治療，オミックス

（受付日：2011年5月19日）