Endogenous Murine AΒ Increases Amyloid Deposition In
Neurobiology of Aging 36 (2015) 2241e2247 Contents lists available at ScienceDirect Neurobiology of Aging journal homepage: www.elsevier.com/locate/neuaging Endogenous murine Ab increases amyloid deposition in APP23 but not in APPPS1 transgenic mice Jasmin Mahler a,b,c, Jose Morales-Corraliza d,e, Julia Stolz a,b,c, Angelos Skodras a,b, Rebecca Radde a, Carmen C. Duma a, Yvonne S. Eisele a,b, Matthew J. Mazzella d, Harrison Wong d, William E. Klunk e,f,g, K. Peter R. Nilsson h, Matthias Staufenbiel a,b, * Paul M. Mathews d,e, Mathias Jucker a,b, , Bettina M. Wegenast-Braun a,b,* a Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany b DZNE, German Center for Neurodegenerative Diseases, Tübingen, Germany c Graduate School for Cellular and Molecular Neuroscience, University of Tübingen, Tübingen, Germany d Center for Dementia Research, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY, USA e Department of Psychiatry, New York University School of Medicine, New York, NY, USA f Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA g Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA h Department of Chemistry, IFM, Linköping University, Linköping, Sweden article info abstract Article history: Endogenous murine amyloid-b peptide (Ab) is expressed in most Ab precursor protein (APP) transgenic Received 18 December 2014 mouse models of Alzheimer’s disease but its contribution to b-amyloidosis remains unclear. We Received in revised form 12 March 2015 demonstrate w35% increased cerebral Ab load in APP23 transgenic mice compared with age-matched Accepted 18 March 2015 APP23 mice on an App-null background.
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