TgCRND8 Amyloid Precursor Protein Transgenic Mice Exhibit an Altered γ-Secretase Processing and an Aggressive, Additive Amyloid Pathology Subject to Immunotherapeutic Modulation-Reference-Cited by-同舟云学术

TgCRND8 Amyloid Precursor Protein Transgenic Mice Exhibit an Altered γ-Secretase Processing and an Aggressive, Additive Amyloid Pathology Subject to Immunotherapeutic Modulation

Published:2007-08-18 Issue:36 Volume:46 Page:10317-10327
ISSN:0006-2960
Container-title:Biochemistry
language:en
Short-container-title:Biochemistry

Author:

Van Vickle Gregory D.¹,Esh Chera L.¹,Kalback Walter M.¹,Patton R. Lyle¹,Luehrs Dean C.¹,Kokjohn Tyler A.¹,Fifield Frederick G.¹,Fraser Paul E.¹,Westaway David¹,McLaurin Joanne¹,Lopez John¹,Brune Daniel¹,Newel Amanda J.¹,Poston Marissa¹,Beach Thomas G.¹,Roher Alex E.¹

Affiliation:

1. The Longtine Center for Molecular Biology and Genetics and W. H. Civin Laboratory of Neuropathology, Sun Health Research Institute, Sun City, Arizona 85351, Department of Microbiology, Midwestern University, Glendale, Arizona 85308, Pathology Section, Sun Health Boswell Hospital, Sun City, Arizona 85851, Centre for Research in Neurodegenerative Diseases, University of Toronto, Ontario M5S 3H2, Canada, and Department of Chemistry and Biochemistry, Arizona State University, Tempe, Arizona 85287

Publisher

American Chemical Society (ACS)

Subject

Biochemistry

Link

https://pubs.acs.org/doi/pdf/10.1021/bi700951u

Reference43 articles.

1. Projections of Alzheimer's disease in the United States and the public health impact of delaying disease onset.

2. Massive CA1/2 Neuronal Loss with Intraneuronal and N-Terminal Truncated Aβ42 Accumulation in a Novel Alzheimer Transgenic Model

3. Early-onset Amyloid Deposition and Cognitive Deficits in Transgenic Mice Expressing a Double Mutant Form of Amyloid Precursor Protein 695

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