Cerebral amyloid angiopathy (CAA), due to vascular amyloid β (Aβ) deposition, is a risk factor for intracerebral haemorrhage and dementia. CAA can occur in sporadic or rare hereditary forms, and is almost invariably associated with Alzheimer’s disease (AD). Experimental (animal) models are of great interest in studying mechanisms and potential treatments for CAA. Naturally occurring animal models of CAA exist, including cats, dogs and non-human primates, which can be used for longitudinal studies. However, due to ethical considerations and low throughput of these models, other animal models are more favourable for research. In the past two decades, a variety of transgenic mouse models expressing the human Aβ precursor protein (APP) has been developed. Many of these mouse models develop CAA in addition to senile plaques, whereas some of these models were generated specifically to study CAA. In addition, other animal models make use of a second stimulus, such as hypoperfusion or hyperhomocysteinemia (HHcy), to accelerate CAA. In this manuscript, we provide a comprehensive review of existing animal models for CAA, which can aid in understanding the pathophysiology of CAA and explore the response to potential therapies.
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October 2017
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In this issue of Clinical Science, Thompson et al (pages 2489-2501) describe their research on the capacity of protein tyrosine phosphatase 1B inhibitor to reverse atherosclerotic plaque formation in a mouse model. The cover image shows aortic root sections of mice fed on a high-fat-diet that are stained with Oil Red - a method the authors used to quantify plaque formation in this study.
Review Article|
September 28 2017
Animal models of cerebral amyloid angiopathy
Lieke Jäkel;
Lieke Jäkel
1Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Departments of Neurology and Laboratory Medicine, Radboud Alzheimer Centre, Nijmegen, The Netherlands
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William E. Van Nostrand;
William E. Van Nostrand
2Department of Neurosurgery, Stony Brook University, Stony Brook, NY, U.S.A.
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James A.R. Nicoll;
James A.R. Nicoll
3Clinical Neurosciences, Clinical and Experimental Sciences, University of Southampton, Southampton, U.K.
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David J. Werring;
David J. Werring
4Department of Brain Repair and Rehabilitation, UCL Stroke Research Centre, UCL Institute of Neurology and the National Hospital for Neurology and Neurosurgery, London, U.K.
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Marcel M. Verbeek
1Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Departments of Neurology and Laboratory Medicine, Radboud Alzheimer Centre, Nijmegen, The Netherlands
Correspondence: Marcel M. Verbeek ([email protected])
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Publisher: Portland Press Ltd
Received:
July 01 2017
Revision Received:
August 24 2017
Accepted:
August 29 2017
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© 2017 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society
2017
Clin Sci (Lond) (2017) 131 (19): 2469–2488.
Article history
Received:
July 01 2017
Revision Received:
August 24 2017
Accepted:
August 29 2017
Citation
Lieke Jäkel, William E. Van Nostrand, James A.R. Nicoll, David J. Werring, Marcel M. Verbeek; Animal models of cerebral amyloid angiopathy. Clin Sci (Lond) 1 October 2017; 131 (19): 2469–2488. doi: https://doi.org/10.1042/CS20170033
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