Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy

Complement C3 Is Activated in Human AD Brain and Is Required for Neurodegeneration in Mouse Models of Amyloidosis and Tauopathy

Summary: Complement pathway overactivation can lead to neuronal damage in various neurological diseases. Although Alzheimer’s disease (AD) is characterized by β-amyloid plaques and tau tangles, previous work examining complement has largely focused on amyloidosis models. We find that glial cells sho...

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Bibliographic Details
Main Authors: Tiffany Wu, Borislav Dejanovic, Vineela D. Gandham, Alvin Gogineni, Rose Edmonds, Stephen Schauer, Karpagam Srinivasan, Melanie A. Huntley, Yuanyuan Wang, Tzu-Ming Wang, Maj Hedehus, Kai H. Barck, Maya Stark, Hai Ngu, Oded Foreman, William J. Meilandt, Justin Elstrott, Michael C. Chang, David V. Hansen, Richard A.D. Carano, Morgan Sheng, Jesse E. Hanson
Format: Article
Language:English
Published: Elsevier 2019-08-01
Series:Cell Reports
Online Access:http://www.sciencedirect.com/science/article/pii/S2211124719309647

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http://www.sciencedirect.com/science/article/pii/S2211124719309647

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