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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Thy1-APPSweArc)BLngn
transgene insertion B, Lars Nilsson
MGI:4420229
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
tg1
Tg(Thy1-APPSweArc)BLngn/0 B6J.Cg-Tg(Thy1-APPSweArc)BLngn MGI:5708587
tg2
Tg(Thy1-APPSweArc)BLngn/0 involves: C57BL/6 * CBA MGI:4420260


Genotype
MGI:5708587
tg1
Allelic
Composition
Tg(Thy1-APPSweArc)BLngn/0
Genetic
Background
B6J.Cg-Tg(Thy1-APPSweArc)BLngn
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• at 14 months of age, mutants are impaired in a passive avoidance learning test, with mice not avoiding the corners as much as controls during the acquisition phase or 24 hours later
• at 14 months of age, mutants require a longer time to habituate the corner visit response when placed inside the IntelliCage environment
• in the object recognition task, mutants explore the objects more during the sample phase
• young mutants show less exploratory behavior than controls during the initial adaptation period to the IntelliCage, showing a lower number of corner visits and visits with licks
• mutants perseverate in place preference extinction test at 4 and 14 months of age
• mice show lower water consumption under basal conditions at 4 months, but not 14 months, of age
• when a novel stimulus (smell at 4 months or aversive air-puffs at 4 months and 14 months) is presented in the familiar environment of IntelliCage, mutants do not inhibit their approaches to the corners as controls do, indicating behavioral disinhibition
• mutants repeat in visiting previously rewarded corners whereas controls are less likely to do so, indicating lower alternation rates and stereotypy

growth/size/body
• reduction in body weight, with the difference in average body weight being 14.8% at 4 months and 27% at 10 months

homeostasis/metabolism
• mice exhibit extensive plaque pathology at 17 months of age

nervous system
• mice exhibit extensive plaque pathology at 17 months of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Alzheimer's disease DOID:10652 J:162999




Genotype
MGI:4420260
tg2
Allelic
Composition
Tg(Thy1-APPSweArc)BLngn/0
Genetic
Background
involves: C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
No mouse lines available in IMSR.
See publication links below for author information.
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• punctate intraneuronal amyloid beta staining is observed frequently in lower layers of the cerebral cortex in 2-month old animals
• mice at 5-6 months display amyloid plaques in the CA1 pyramidal cell layer of the hippocampus, with enhanced intraneuronal amyloid beta aggregates detectable at 4 months (increasing further until most animals have plaques at 6 months); accumulation of amyloid beta aggregates begins prior to plaque formation
• at 9 months of age, granular intraneuronal amyloid beta aggregates were frequent and widespread in (lower layers of ) the cerebral cortex, subiculum and CA1 hippocampal region; amyloid plaques are also observed in thalamic nuclei although APP expression is low
• cerebral amyloid deposition is seen in animals with high plaque load but this is not a prominent feature in mutants
• amyloid deposits are surrounded by marked astrogliosis

homeostasis/metabolism
• punctate intraneuronal amyloid beta staining is observed frequently in lower layers of the cerebral cortex in 2-month old animals
• mice at 5-6 months display amyloid plaques in the CA1 pyramidal cell layer of the hippocampus, with enhanced intraneuronal amyloid beta aggregates detectable at 4 months (increasing further until most animals have plaques at 6 months); accumulation of amyloid beta aggregates begins prior to plaque formation
• at 9 months of age, granular intraneuronal amyloid beta aggregates were frequent and widespread in (lower layers of ) the cerebral cortex, subiculum and CA1 hippocampal region; amyloid plaques are also observed in thalamic nuclei although APP expression is low
• cerebral amyloid deposition is seen in animals with high plaque load but this is not a prominent feature in mutants





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory