mortality/aging
• 47.1% of animals died by 180 days of age; mortality by 360 days is 70.6% compared to 4.3% in controls
|
nervous system
• diffuse amyloid plaques and compact neuritic plaques are detected in all mice 13-18 months old, most abundant in the hippocampus and cortex while occasionally seen in the thalamus, fimbria, external capsule, pontine nuclei, and white matter; plaques contain high amounts of the Abeta 42 peptidediffuse amyloid plaques and compact neuritic plaques are detected in all mice 13-18 months old, most abundant in the hippocampus and cortex while occasionally seen in the thalamus, fimbria, external capsule, pontine nuclei, and white matter; plaques contain high amounts of the Abeta 42 peptide
(J:53800)
• mice younger than 12 months do not exhibit amyloid deposits
(J:53800)
• levels of plaque peptides extracted with guanidinium hydrochloride increase exponentially in mutants >15 months of age; plaque associated peptides are not detected in brains of mice at 6-9 months of age
(J:64209)
• subiculum region of brain is loaded amyloid deposits starting at 10 months of age
(J:93635)
|
• amyloid deposits are found in the parenchyma and in cortical and leptimenigeal arterioles in brains at 16 months
|
• by 15 months, subiculum is almost totally covered with diffuse and senile plaques
|
• dystrophic neurites with swollen and distorted neuritic profiles are identified in brains of mice
|
• tetanic stimulation in hippocampal brain slices triggers significantly impaired LTP; LTP progressively decreases in brain slices
(J:87229)
|
behavior/neurological
• ambulation measured in a corner-crossing variant upon transfer to a new cage is reduced relative to controls at 4-9 weeks of age, 12-17, and 20-52 weeks with differences becoming more pronounced with age
|
hyperactivity
(
J:53800
)
• mice exhibit increased episodes of agitation and spontaneous activity by 8 weeks of age onward
|
homeostasis/metabolism
• in brains of 10-12 month-old mice, diffuse and senile amyloid plaques are present and increase exponentially with age
(J:87229)
|
• diffuse amyloid plaques and compact neuritic plaques are detected in all mice 13-18 months old, most abundant in the hippocampus and cortex while occasionally seen in the thalamus, fimbria, external capsule, pontine nuclei, and white matter; plaques contain high amounts of the Abeta 42 peptidediffuse amyloid plaques and compact neuritic plaques are detected in all mice 13-18 months old, most abundant in the hippocampus and cortex while occasionally seen in the thalamus, fimbria, external capsule, pontine nuclei, and white matter; plaques contain high amounts of the Abeta 42 peptide
(J:53800)
• mice younger than 12 months do not exhibit amyloid deposits
(J:53800)
• levels of plaque peptides extracted with guanidinium hydrochloride increase exponentially in mutants >15 months of age; plaque associated peptides are not detected in brains of mice at 6-9 months of age
(J:64209)
• subiculum region of brain is loaded amyloid deposits starting at 10 months of age
(J:93635)
|
• amyloid deposits are found in the parenchyma and in cortical and leptimenigeal arterioles in brains at 16 months
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
Alzheimer's disease | DOID:10652 | J:93635 |