PMID- 28963121
OWN - NLM
STAT- MEDLINE
DCOM- 20171010
LR  - 20171010
IS  - 1470-8736 (Electronic)
IS  - 0143-5221 (Linking)
VI  - 131
IP  - 19
DP  - 2017 Oct 15
TI  - Animal models of cerebral amyloid angiopathy.
PG  - 2469-2488
LID - 10.1042/CS20170033 [doi]
AB  - Cerebral amyloid angiopathy (CAA), due to vascular amyloid beta (Abeta) 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 Abeta 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.
CI  - (c) 2017 The Author(s). Published by Portland Press Limited on behalf of the 
      Biochemical Society.
FAU - Jakel, Lieke
AU  - Jakel L
AD  - Radboud University Medical Center, Donders Institute for Brain, Cognition and 
      Behaviour, Departments of Neurology and Laboratory Medicine, Radboud Alzheimer 
      Centre, Nijmegen, The Netherlands.
FAU - Van Nostrand, William E
AU  - Van Nostrand WE
AD  - Department of Neurosurgery, Stony Brook University, Stony Brook, NY, U.S.A.
FAU - Nicoll, James A R
AU  - Nicoll JAR
AD  - Clinical Neurosciences, Clinical and Experimental Sciences, University of 
      Southampton, Southampton, U.K.
FAU - Werring, David J
AU  - Werring DJ
AD  - 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.
FAU - Verbeek, Marcel M
AU  - Verbeek MM
AD  - Radboud University Medical Center, Donders Institute for Brain, Cognition and 
      Behaviour, Departments of Neurology and Laboratory Medicine, Radboud Alzheimer 
      Centre, Nijmegen, The Netherlands marcel.verbeek@radboudumc.nl.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170928
PL  - England
TA  - Clin Sci (Lond)
JT  - Clinical science (London, England : 1979)
JID - 7905731
RN  - 0 (APP protein, human)
RN  - 0 (Amyloid beta-Protein Precursor)
SB  - IM
MH  - Amyloid beta-Protein Precursor/genetics/*metabolism
MH  - Animals
MH  - Brain/*metabolism/pathology/physiopathology
MH  - Cerebral Amyloid Angiopathy/genetics/*metabolism/pathology/physiopathology
MH  - Disease Models, Animal
MH  - Genetic Predisposition to Disease
MH  - Humans
MH  - Mice, Transgenic
MH  - Phenotype
MH  - Plaque, Amyloid
MH  - Species Specificity
OTO - NOTNLM
OT  - Amyloid-beta
OT  - Animal models
OT  - Cerebral amyloid angiopathy
OT  - Transgenic mice
EDAT- 2017/10/01 06:00
MHDA- 2017/10/11 06:00
CRDT- 2017/10/01 06:00
PHST- 2017/07/01 00:00 [received]
PHST- 2017/08/24 00:00 [revised]
PHST- 2017/08/29 00:00 [accepted]
PHST- 2017/10/01 06:00 [entrez]
PHST- 2017/10/01 06:00 [pubmed]
PHST- 2017/10/11 06:00 [medline]
AID - CS20170033 [pii]
AID - 10.1042/CS20170033 [doi]
PST - epublish
SO  - Clin Sci (Lond). 2017 Sep 28;131(19):2469-2488. doi: 10.1042/CS20170033. Print 
      2017 Oct 15.