ApoE4 markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy

Yang Shi, Kaoru Yamada, Shane Antony Liddelow, Scott T. Smith, Lingzhi Zhao, Wenjie Luo, Richard M. Tsai, Salvatore Spina, Lea T. Grinberg, Julio C. Rojas, Gilbert Gallardo, Kairuo Wang, Joseph Roh, Grace Robinson, Mary Beth Finn, Hong Jiang, Patrick M. Sullivan, Caroline Baufeld, Michael W. Wood, Courtney Sutphen, Lena McCue, Chengjie Xiong, Jorge L. Del-Aguila, John C. Morris, Carlos Cruchaga, Anne M. Fagan, Bruce L. Miller, Adam L. Boxer, William W. Seeley, Oleg Butovsky, Ben A. Barres, Steven M. Paul and David M. Holtzman ()
Additional contact information
Yang Shi: Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine
Kaoru Yamada: Graduate School of Medicine, The University of Tokyo
Shane Antony Liddelow: School of Medicine, Stanford University
Scott T. Smith: Brigham and Women’s Hospital, Harvard Medical School
Lingzhi Zhao: Appel Alzheimer’s Disease Research Institute, Feil Family Brain and Mind Research Institute, Weill Cornell Medical College of Cornell University
Wenjie Luo: Appel Alzheimer’s Disease Research Institute, Feil Family Brain and Mind Research Institute, Weill Cornell Medical College of Cornell University
Richard M. Tsai: Memory and Aging Center, University of California
Salvatore Spina: Memory and Aging Center, University of California
Lea T. Grinberg: Memory and Aging Center, University of California
Julio C. Rojas: Memory and Aging Center, University of California
Gilbert Gallardo: Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine
Kairuo Wang: Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine
Joseph Roh: Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine
Grace Robinson: University of Missouri School of Medicine
Mary Beth Finn: Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine
Hong Jiang: Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine
Patrick M. Sullivan: Duke University Medical Center, Durham Veterans Health Administration Medical Center’s Geriatric Research, Education and Clinical Center
Caroline Baufeld: Brigham and Women’s Hospital, Harvard Medical School
Michael W. Wood: AstraZeneca R&D
Courtney Sutphen: Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine
Lena McCue: Washington University in St Louis
Chengjie Xiong: Washington University in St Louis
Jorge L. Del-Aguila: Washington University School of Medicine
John C. Morris: Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine
Carlos Cruchaga: Washington University School of Medicine
Anne M. Fagan: Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine
Bruce L. Miller: Memory and Aging Center, University of California
Adam L. Boxer: Memory and Aging Center, University of California
William W. Seeley: Memory and Aging Center, University of California
Oleg Butovsky: Brigham and Women’s Hospital, Harvard Medical School
Ben A. Barres: School of Medicine, Stanford University
Steven M. Paul: Voyager Therapeutics
David M. Holtzman: Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University School of Medicine

Nature, 2017, vol. 549, issue 7673, 523-527

Abstract: ApoE4 exacerbates tau pathogenesis, neuroinflammation and tau-mediated neurodegeneration independently of brain amyloid-β pathology, and exerts a ‘toxic’ gain of function whereas its absence is protective.

Date: 2017
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DOI: 10.1038/nature24016

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