Novel App knock-in mouse model shows key features of amyloid pathology and reveals profound metabolic dysregulation of microglia

Abstract Background Genetic mutations underlying familial Alzheimer’s disease (AD) were identified decades ago, but the field is still in search of transformative therapies for patients. While mouse models based on overexpression of mutated transgenes have yielded key insights in mechanisms of disea...

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Váldodahkkit:	Dan Xia, Steve Lianoglou, Thomas Sandmann, Meredith Calvert, Jung H. Suh, Elliot Thomsen, Jason Dugas, Michelle E. Pizzo, Sarah L. DeVos, Timothy K. Earr, Chia-Ching Lin, Sonnet Davis, Connie Ha, Amy Wing-Sze Leung, Hoang Nguyen, Roni Chau, Ernie Yulyaningsih, Isabel Lopez, Hilda Solanoy, Shababa T. Masoud, Chun-chi Liang, Karin Lin, Giuseppe Astarita, Nathalie Khoury, Joy Yu Zuchero, Robert G. Thorne, Kevin Shen, Stephanie Miller, Jorge J. Palop, Dylan Garceau, Michael Sasner, Jennifer D. Whitesell, Julie A. Harris, Selina Hummel, Johannes Gnörich, Karin Wind, Lea Kunze, Artem Zatcepin, Matthias Brendel, Michael Willem, Christian Haass, Daniel Barnett, Till S. Zimmer, Anna G. Orr, Kimberly Scearce-Levie, Joseph W. Lewcock, Gilbert Di Paolo, Pascal E. Sanchez
Materiálatiipa:	Artigo
Giella:	Inglês
Almmustuhtton:	BMC 2022-06-01
Ráidu:	Molecular Neurodegeneration
Fáttát:	Neuritic plaques Vascular amyloid Neurodegeneration Astrogliosis Phagocytic microglia Lipid dyshomeostasis
Liŋkkat:	https://doi.org/10.1186/s13024-022-00547-7
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