Production of seedable Amyloid-β peptides in model of prion diseases upon PrPSc-induced PDK1 overactivation

Aβ plaques have been detected in brains of patients with prion diseases. Here, using mice, the authors show that prion infection enhances Aβ production via a PDK1-TACE mechanism and that brain deposition of Aβ induced by Aβ seeds co-transmitted with PrPSc contributes to mortality in prion disease....

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Autores principales: Juliette Ezpeleta, Vincent Baudouin, Zaira E. Arellano-Anaya, François Boudet-Devaud, Mathéa Pietri, Anne Baudry, Anne-Marie Haeberlé, Yannick Bailly, Odile Kellermann, Jean-Marie Launay, Benoit Schneider
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2019
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Acceso en línea:https://doaj.org/article/1e4e707388e247a5aac2217f5c04838e
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Sumario:Aβ plaques have been detected in brains of patients with prion diseases. Here, using mice, the authors show that prion infection enhances Aβ production via a PDK1-TACE mechanism and that brain deposition of Aβ induced by Aβ seeds co-transmitted with PrPSc contributes to mortality in prion disease.