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Animal models of cerebral amyloid angiopathy.

Authors
  • Jäkel, Lieke1
  • Van Nostrand, William E2
  • Nicoll, James A R3
  • Werring, David J4
  • Verbeek, Marcel M5
  • 1 Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Departments of Neurology and Laboratory Medicine, Radboud Alzheimer Centre, Nijmegen, The Netherlands. , (Netherlands)
  • 2 Department of Neurosurgery, Stony Brook University, Stony Brook, NY, U.S.A.
  • 3 Clinical Neurosciences, Clinical and Experimental Sciences, University of Southampton, Southampton, U.K.
  • 4 Department of Brain Repair and Rehabilitation, UCL Stroke Research Centre, UCL Institute of Neurology and the National Hospital for Neurology and Neurosurgery, London, U.K.
  • 5 Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Departments of Neurology and Laboratory Medicine, Radboud Alzheimer Centre, Nijmegen, The Netherlands [email protected] , (Netherlands)
Type
Published Article
Journal
Clinical Science
Publisher
Portland Press
Publication Date
Oct 15, 2017
Volume
131
Issue
19
Pages
2469–2488
Identifiers
DOI: 10.1042/CS20170033
PMID: 28963121
Source
Medline
Keywords
License
Unknown

Abstract

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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