Analysis Tools
behavior/neurological
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• 6-8 month old mutants show increased latencies to locate the hidden platform in the Morris water maze indicating a learning deficit
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• 12- and 18-month old mutants show impaired probe trial performance, indicating a memory impairment
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cardiovascular system
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• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels
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• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness
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• middle cerebral arteries show a 50% loss of ability to dilate in response to acetylcholine and calcitonin gene-related peptide compared to wild-type vessels
• arterial dysfunction is not due to oxidative stress
• by 18 months of age, mutants exhibit impaired maximal diameter decrease during NOS inhibition with N-nitro-L-arginine
• however, contractile response of arteries to endothelin-1 is normal
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muscle
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• middle cerebral arteries show a 50% loss of ability to dilate in response to acetylcholine and calcitonin gene-related peptide compared to wild-type vessels
• arterial dysfunction is not due to oxidative stress
• by 18 months of age, mutants exhibit impaired maximal diameter decrease during NOS inhibition with N-nitro-L-arginine
• however, contractile response of arteries to endothelin-1 is normal
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nervous system
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• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness
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• mutants exhibit age-dependent amyloid beta plaque deposition in the cortex and hippocampus; 18 month old mutants exhibit parenchymal amyloid beta senile plaques
• mutants exhibit increased levels of soluble and insoluble amyloid beta(1-40) and amyloid beta(1-42) between 6-8 and 12 months of age and further increases in amyloid beta(1-40) at 18 months of age, in the cortex
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• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels
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astrocytosis
(
J:167619
)
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• mutants exhibit activated GFAP-positive astrocytes in the cortex; activated astrocytes are distributed in clusters as well as diffusely throughout the cortex
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• mutants exhibit significant collagen accumulation in the surface pial membrane, resulting in increased thickness
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• about 22-23% reduction in the number of cortical cholinergic fibers in adults and aged-mutants
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• glucose uptake is impaired in activated somatosensory cortex of aged mutants after whisker stimulation
• gradual loss of the neuronally-driven hemodynamic response to sensory whisker stimulation
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homeostasis/metabolism
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• mutants exhibit age-dependent amyloid beta plaque deposition in the cortex and hippocampus; 18 month old mutants exhibit parenchymal amyloid beta senile plaques
• mutants exhibit increased levels of soluble and insoluble amyloid beta(1-40) and amyloid beta(1-42) between 6-8 and 12 months of age and further increases in amyloid beta(1-40) at 18 months of age, in the cortex
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• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| Alzheimer's disease | DOID:10652 | J:167619 | ||
