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Phenotypes Associated with This Genotype
Genotype
MGI:3717577
Allelic
Composition
Tg(Thy1-APPLon)2Vln/0
Genetic
Background
involves: FVB/N
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phenotype observed in females
phenotype observed in males
N normal phenotype
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
• less than 15% of mice older than 6 months display spontaneous seizures
• 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
• mice exhibit increased episodes of agitation and spontaneous activity by 8 weeks of age onward
• less than 15% of mice older than 6 months display spontaneous seizures

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 OMIM:104300
OMIM:502500
OMIM:604154
OMIM:608907
J:93635


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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last database update
04/18/2017
MGI 6.08
The Jackson Laboratory