scholarly journals Development of Cerebral Microbleeds in the APP23-Transgenic Mouse Model of Cerebral Amyloid Angiopathy—A 9.4 Tesla MRI Study

2016 ◽  
Vol 8 ◽  
Author(s):  
Björn Reuter ◽  
Alexander Venus ◽  
Patrick Heiler ◽  
Lothar Schad ◽  
Anne Ebert ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Cerebral Amyloid Angiopathy ◽  
Transgenic Mouse Model ◽  
Cerebral Microbleeds ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid ◽  
Mri Study

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 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

Abstract W MP94: Acute Inflammation Expands Cerebral Microbleeds in a Mouse Model of Cerebral Amyloid Angiopathy

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Vitaly Vasilevko ◽  
Mark J Fisher ◽  
Kelley Kilday ◽  
Giselle F Passos ◽  
Shuo Liu ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mice ◽  
Cerebral Amyloid Angiopathy ◽  
Acute Inflammation ◽  
Cerebral Microbleeds ◽  
High Dose ◽  
Amyloid Angiopathy ◽  
Inflammatory Stimulus ◽  
Cerebral Amyloid ◽  
Average Size

Introduction: Cerebral microscopic hemorrhages are the pathologic substrate of cerebral microbleeds (CMB). Little is known about mechanisms of expansion of CMB. Here we studied the dynamics of CMB after acute inflammation, using a transgenic mouse model of cerebral amyloid angiopathy with spontaneous microscopic hemorrhages and endotoxin (lipopolysaccharide, LPS) as an inflammatory stimulus. Methods: 21-month old Tg2576 mice and wildtype littermates received a single dose of LPS, 100 or 1000 ug/kg i.p., or phosphate-buffered saline (PBS) as control. Mice were sacrificed 48 hours later and brains were collected for the analysis of microscopic hemorrhages, as well as edema formation, blood-brain barrier constituents and glial activation. Differences among groups were tested by anova and contrasts. Results: Hematoxylin and eosin staining demonstrated no freshly-formed microscopic hemorrhages in LPS-treated mice. Using Prussian blue staining, we found that total area, average size, and number of CMB differed significantly between PBS-treated wildtype and transgenic mice (p=0.03, p=.04 and p=.03 respectively). Acute inflammation did not significantly affect total area, average size, or number of CMB in wildtype animals. For transgenic mice, both doses of LPS significantly (p<.01) increased the total area of Prussian blue-positive lesions (2.2 to 2.9-fold increase), and higher LPS dose significantly (p<.01) increased average size of CMB by 2.6-fold; both average and total size of CMB increased in a dose-dependent manner. IgG and fibrinogen levels significantly increased after high dose LPS injection in both wildtype and transgenic mice (p<.05). Tight junction protein claudin-5 levels were also increased in high dose LPS-treated mice (p<0.05). LPS injection significantly increased expression of activated microglia markers CD45, CD14, and Iba1. Conclusions: In a mouse model of cerebral amyloid angiopathy, acute inflammatory stimulus induced expansion of CMB without producing fresh hemorrhage. Increased size of CMB was associated with indices of cerebral edema, alteration of tight junction constituents, and microglial activation. These findings suggest that cerebral edema may mediate expansion of cerebral microbleeds.

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