Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice

被引：0

作者：

Johannes Steffen

Markus Krohn

Christina Schwitlick

Thomas Brüning

Kristin Paarmann

Claus U. Pietrzik

Henrik Biverstål

Baiba Jansone

Oliver Langer

Jens Pahnke

机构：

[1] University of Oslo (UiO) / Oslo Universiy Hospital (OUS),Translational Neurodegeneration Research and Neuropathology Lab

[2] University of Lübeck (UzL),Institute for Pathobiochemistry

[3] LIED,Department of Physical Organic Chemistry

[4] Leibniz Institute for of Plant Biochemistry (IPB),Faculty of Medicine, Department of Pharmacology

[5] University Medical Center of the Johannes-Gutenberg-University,Department of Clinical Pharmacology

[6] Latvian Institute of Organic Synthesis (OSI),undefined

[7] University of Latvia (LU),undefined

[8] Center for Health & Bioresources,undefined

[9] Austrian Institute of Technology GmbH (AIT),undefined

[10] Medical University of Vienna,undefined

来源：

Acta Neuropathologica Communications | / 5卷

关键词：

Murine amyloid-beta; Abeta; Transgenic mice; Amyloid precursor protein; Alzheimer’s disease; Amyloidosis;

D O I：

暂无

中图分类号：

学科分类号：

摘要：

Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer’s disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ and enhancing cognition in mice but failed totally in human. One model-dependent factor has so far been almost completely neglected: the endogenous expression of mouse APP and its effects on the transgenic models and the readout for therapeutic approaches.

引用

共 325 条

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