scholarly journals Murine versus human apolipoprotein E4: differential facilitation of and co-localization in cerebral amyloid angiopathy and amyloid plaques in APP transgenic mouse models

2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Fan Liao ◽  
Tony J. Zhang ◽  
Hong Jiang ◽  
Katheryn B. Lefton ◽  
Grace O. Robinson ◽  
...  
Keyword(s):  
Transgenic Mouse ◽  
Mouse Models ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Plaques ◽  
Amyloid Angiopathy ◽  
Transgenic Mouse Models ◽  
Apolipoprotein E4 ◽  
Human Apolipoprotein ◽  
Cerebral Amyloid

Transgenic Mouse Models of Cerebral Amyloid Angiopathy

2001 ◽  
pp. 123-128 ◽  
Author(s):  
Martin C. Herzig ◽  
David T. Winkler ◽  
Lary C. Walker ◽  
Mathias Jucker
Keyword(s):  
Transgenic Mouse ◽  
Mouse Models ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Transgenic Mouse Models ◽  
Cerebral Amyloid

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 Hereditary cerebral amyloid angiopathy, Piedmont-type mutation

2020 ◽  
Vol 6 (2) ◽  
pp. e411 ◽  
Author(s):  
Mariel G. Kozberg ◽  
Susanne J. van Veluw ◽  
Matthew P. Frosch ◽  
Steven M. Greenberg
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Ex Vivo ◽  
Amyloid Plaques ◽  
Amyloid Angiopathy ◽  
Pathologic Examination ◽  
Potential Association ◽  
History Of ◽  
Intracerebral Hemorrhages ◽  
Β Amyloid ◽  
Cerebral Amyloid

ObjectiveWe present here a case report of a patient with a family history of intracerebral hemorrhages (ICHs) who presented with multiple large lobar hemorrhages in rapid succession, with cognitive sparing, who was found to have a mutation in the β-amyloid coding sequence of amyloid precursor protein (Leu705Val), termed the Piedmont-type mutation, the second ever reported case of this form of hereditary cerebral amyloid angiopathy (CAA).MethodsTargeted pathologic examination was performed aided by the use of ex vivo MRI.ResultsSevere CAA was observed mainly involving the leptomeningeal vessels and, to a far lesser extent, cortical vessels, with no amyloid plaques or neurofibrillary tangles.ConclusionsThis leptomeningeal pattern of β-amyloid deposition coupled with multiple large hemorrhages demonstrates unique pathophysiologic characteristics of CAA associated with the Piedmont-type mutation, suggesting a potential association between leptomeningeal CAA and larger ICHs.

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%.

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