S3-01-06 Cerebral amyloid angiopathy in transgenic mouse models

2004 ◽  
Vol 25 ◽  
pp. S46-S47
Author(s):  
Mathias Jucker ◽  
Matthias Staufenbiel ◽  
Paul Mathews
Keyword(s):  
Transgenic Mouse ◽  
Mouse Models ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Transgenic Mouse Models ◽  
Cerebral Amyloid

scholarly journals Progression of Cerebral Amyloid Angiopathy in Transgenic Mouse Models of Alzheimer Disease

2005 ◽  
Vol 64 (7) ◽  
pp. 588-594 ◽  
Author(s):  
Sarah B Domnitz ◽  
Elissa M Robbins ◽  
Alex W Hoang ◽  
Monica Garcia-Alloza ◽  
Bradley T Hyman ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Transgenic Mouse Models ◽  
Cerebral Amyloid

scholarly journals Animal models of cerebral amyloid angiopathy

2017 ◽  
Vol 131 (19) ◽  
pp. 2469-2488 ◽  
Author(s):  
Lieke Jäkel ◽  
William E. Van Nostrand ◽  
James A.R. Nicoll ◽  
David J. Werring ◽  
Marcel M. Verbeek
Keyword(s):  
Animal Models ◽  
Mouse Models ◽  
Cerebral Amyloid Angiopathy ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Transgenic Mouse Models ◽  
Ethical Considerations ◽  
Naturally Occurring ◽  
Cerebral Amyloid

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.

scholarly journals Secondary Metabolites from Plants Possessing Inhibitory Properties against Beta-Amyloid Aggregation as Revealed by Thioflavin-T Assay and Correlations with Investigations on Transgenic Mouse Models of Alzheimer’s Disease

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 870 ◽  
Author(s):  
Raluca Stefanescu ◽  
Gabriela Dumitriṭa Stanciu ◽  
Andrei Luca ◽  
Luminita Paduraru ◽  
Bogdan-Ionel Tamba
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Secondary Metabolites ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Beta Amyloid ◽  
Thioflavin T ◽  
Amyloid Angiopathy ◽  
Transgenic Mouse Models ◽  
Study Results

Alzheimer’s disease is a neurodegenerative disorder for which there is a continuous search of drugs able to reduce or stop the cognitive decline. Beta-amyloid peptides are composed of 40 and 42 amino acids and are considered a major cause of neuronal toxicity. They are prone to aggregation, yielding oligomers and fibrils through the inter-molecular binding between the amino acid sequences (17–42) of multiple amyloid-beta molecules. Additionally, amyloid deposition causes cerebral amyloid angiopathy. The present study aims to identify, in the existing literature, natural plant derived products possessing inhibitory properties against aggregation. The studies searched proved the anti-aggregating effects by the thioflavin T assay and through behavioral, biochemical, and histological analysis carried out upon administration of natural chemical compounds to transgenic mouse models of Alzheimer’s disease. According to our present study results, fifteen secondary metabolites from plants were identified which presented both evidence coming from the thioflavin T assay and transgenic mouse models developing Alzheimer’s disease and six additional metabolites were mentioned due to their inhibitory effects against fibrillogenesis. Among them, epigallocatechin-3-gallate, luteolin, myricetin, and silibinin were proven to lower the aggregation to less than 40%.

MEMANTINE ATTENUATES VASCULAR AMYLOID β DEPOSITS AND SPONTANEOUS HEMORRHAGES IN MOUSE MODELS OF CEREBRAL AMYLOID ANGIOPATHY

2017 ◽  
Vol 13 (7) ◽  
pp. P917-P918 ◽  
Author(s):  
Yasuteru Inoue ◽  
Mitsuharu Ueda ◽  
Teruaki Masuda ◽  
Yohei Misumi ◽  
Taro Yamashita ◽  
...  
Keyword(s):  
Mouse Models ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

scholarly journals Environmental Enrichment: Disentangling the Influence of Novelty, Social, and Physical Activity on Cerebral Amyloid Angiopathy in a Transgenic Mouse Model

2020 ◽  
Vol 21 (3) ◽  
pp. 843
Author(s):  
Lisa S. Robison ◽  
Nikita Francis ◽  
Dominique L. Popescu ◽  
Maria E. Anderson ◽  
Joshua Hatfield ◽  
...  
Keyword(s):  
Physical Activity ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Cerebral Amyloid Angiopathy ◽  
Environmental Enrichment ◽  
Transgenic Mouse Model ◽  
Cognitive Stimulation ◽  
Cognitive Behavioral ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

Cerebral amyloid angiopathy (CAA) is the deposition of amyloid protein in the cerebral vasculature, a common feature in both aging and Alzheimer’s disease (AD). However, the effects of environmental factors, particularly cognitive stimulation, social stimulation, and physical activity, on CAA pathology are poorly understood. These factors, delivered in the form of the environmental enrichment (EE) paradigm in rodents, have been shown to have beneficial effects on the brain and behavior in healthy aging and AD models. However, the relative importance of these subcomponents on CAA pathology has not been investigated. Therefore, we assessed the effects of EE, social enrichment (SOC), and cognitive enrichment (COG) compared to a control group that was single housed without enrichment (SIN) from 4 to 8 months of age in wild-type mice (WT) and Tg-SwDI mice, a transgenic mouse model of CAA that exhibits cognitive/behavioral deficits. The results show that individual facets of enrichment can affect an animal model of CAA, though the SOC and combined EE conditions are generally the most effective at producing physiological, cognitive/behavioral, and neuropathological changes, adding to a growing literature supporting the benefits of lifestyle interventions.

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