scholarly journals Age-dependent cerebrovascular dysfunction in a transgenic mouse model of cerebral amyloid angiopathy

Brain ◽  
2007 ◽  
Vol 130 (9) ◽  
pp. 2310-2319 ◽  
Author(s):  
H. K. Shin ◽  
P. B. Jones ◽  
M. Garcia-Alloza ◽  
L. Borrelli ◽  
S. M. Greenberg ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Cerebral Amyloid Angiopathy ◽  
Transgenic Mouse Model ◽  
Amyloid Angiopathy ◽  
Cerebrovascular Dysfunction ◽  
Age Dependent ◽  
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.

scholarly journals Age-Dependent Neurovascular Dysfunction and Damage in a Mouse Model of Cerebral Amyloid Angiopathy

Stroke ◽  
2014 ◽  
Vol 45 (6) ◽  
pp. 1815-1821 ◽  
Author(s):  
Laibaik Park ◽  
Kenzo Koizumi ◽  
Sleiman El Jamal ◽  
Ping Zhou ◽  
Mary Lou Previti ◽  
...  
Keyword(s):  
Mouse Model ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Age Dependent ◽  
Cerebral Amyloid ◽  
Neurovascular Dysfunction

Deletion of murine tau gene increases tau aggregation in a human mutant tau transgenic mouse model

2010 ◽  
Vol 38 (4) ◽  
pp. 1001-1005 ◽  
Author(s):  
Kunie Ando ◽  
Karelle Leroy ◽  
Céline Heraud ◽  
Anna Kabova ◽  
Zehra Yilmaz ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Double Mutant ◽  
Transgenic Mouse Model ◽  
Tau Proteins ◽  
Dependent Manner ◽  
Age Dependent ◽  
Ad Alzheimer’S Disease ◽  
Tau Aggregation ◽  
The Brain

We have reported previously a tau transgenic mouse model (Tg30tau) overexpressing human 4R1N double-mutant tau (P301S and G272V) and that develops AD (Alzheimer's disease)-like NFTs (neurofibrillary tangles) in an age-dependent manner. Since murine tau might interfere with the toxic effects of human mutant tau, we set out to analyse the phenotype of our Tg30tau model in the absence of endogenous murine tau with the aim to reproduce more faithfully a model of human tauopathy. By crossing the Tg30tau line with TauKO (tau-knockout) mice, we have obtained a new mouse line called Tg30×TauKO that expresses only exogenous human double-mutant 4R1N tau. Whereas Tg30×TauKO mice express fewer tau proteins compared with Tg30tau, they exhibit augmented sarkosyl-insoluble tau in the brain and an increased number of Gallyas-positive NFTs in the hippocampus. Taken together, exclusion of murine tau causes accelerated tau aggregation during aging of this mutant tau transgenic model.

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