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Mano, Tatsuo; Nagata, Kenichi; Nonaka, Takashi; Tarutani, Airi; Imamura, Tomohiro; Hashimoto, Tadafumi; Bannai, Taro; Koshi-Mano, Kagari; Tsuchida, Takeyuki; Ohtomo, Ryo; Takahashi-Fujigasaki, Junko; Yamashita, Satoshi; Ohyagi, Yasumasa; Yamasaki, Ryo; Tsuji, Shoji; Tamaoka, Akira; Ikeuchi, Takeshi; Saido, Takaomi C.; Iwatsubo, Takeshi; Ushijima, Toshikazu; Murayama, Shigeo; Hasegawa, Masato; Iwata, Atsushi

Neuron-specific methylome analysis reveals epigenetic regulation and tau-related dysfunction of BRCA1 in Alzheimer’s disease

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  • Medientyp: E-Artikel
  • Titel: Neuron-specific methylome analysis reveals epigenetic regulation and tau-related dysfunction of BRCA1 in Alzheimer’s disease
  • Beteiligte: Mano, Tatsuo; Nagata, Kenichi; Nonaka, Takashi; Tarutani, Airi; Imamura, Tomohiro; Hashimoto, Tadafumi; Bannai, Taro; Koshi-Mano, Kagari; Tsuchida, Takeyuki; Ohtomo, Ryo; Takahashi-Fujigasaki, Junko; Yamashita, Satoshi; Ohyagi, Yasumasa; Yamasaki, Ryo; Tsuji, Shoji; Tamaoka, Akira; Ikeuchi, Takeshi; Saido, Takaomi C.; Iwatsubo, Takeshi; Ushijima, Toshikazu; Murayama, Shigeo; Hasegawa, Masato; Iwata, Atsushi
  • Erschienen: Proceedings of the National Academy of Sciences, 2017
  • Erschienen in: Proceedings of the National Academy of Sciences
  • Sprache: Englisch
  • DOI: 10.1073/pnas.1707151114
  • ISSN: 0027-8424; 1091-6490
  • Schlagwörter: Multidisciplinary
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:title>Significance</jats:title> <jats:p> To extract critical information from Alzheimer’s disease (AD) postmortem brains that may otherwise be lost, we chose to screen epigenetic signatures. Epigenome analysis is a robust methodology in terms of its cell type and gene specificity, suitability for high-throughput analysis, and resistance to postmortem degradation. Analysis of the neuron-specific methylome revealed a variety of differentially methylated genes, including <jats:italic>BRCA1</jats:italic> . We demonstrate the pathogenic relevance of compromised genomic integrity by analyzing the neuroprotective function of BRCA1 against amyloid β (Aβ)-induced DNA double-strand breaks. Furthermore, insolubility of BRCA1 under the presence of aggregated tau suggested the reason for its dysfunction despite enhanced expression. We provide insight into the pathomechanism of AD and demonstrate the potential of screening neuron-specific methylome to reveal new pathogenic contributors. </jats:p>
  • Zugangsstatus: Freier Zugang