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Phenotypes Associated with This Genotype
Genotype
MGI:3709152
Allelic
Composition
Tg(Camk2a-tTA)1Mmay/0
Tg(tetO-APPSwInd)107Dbo/0
Genetic
Background
involves: C3H/HeJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Camk2a-tTA)1Mmay mutation (6 available)
Tg(tetO-APPSwInd)107Dbo mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• doxycycline-mediated suppression of transgenic APPSwInd synthesis leads to parallel reductions of amyloid beta peptide levels (J:109829)
• early onset amyloid formation is observed, with plaques observed as early as 8 weeks of age in mice receiving no doxycycline (DOX) treatment (J:109829)
• plaques are restricted to the forebrain, including the cortex, hippocampus, olfactory bulb, and striatum; by 6 months, amyloid burden covers large cortical and hippocampal areas (J:109829)
• first observed plaques are fibrillar-core deposits; in 6 month old animals, diffuse plaques are apparent and these are abundant at 9 months, while in 9-12 month-old mice, plaques are visible in the thalamus (J:109829)
• no lesions are observed in the cerebellum or brain stem (J:109829)
• animals receiving no treatment display moderate amyloid pathology at 6 months, which progresses to a severe amyloid burden by 9 months (J:109829)
• mice raised for 6 months with no (DOX) treatment, followed by 3 or 6 months of DOX treatment show similar pathology to untreated 6-month old animals, despite relatively long lesion clearance times (J:109829)
• doxycycline-mediated suppression of transgenic APPSwInd synthesis leads to parallel reductions of amyloid beta peptide levels (J:109829)
• early onset amyloid formation is observed, with plaques observed as early as 8 weeks of age in mice receiving no doxycycline (DOX) treatment (J:109829)
• plaques are restricted to the forebrain, including the cortex, hippocampus, olfactory bulb, and striatum; by 6 months, amyloid burden covers large cortical and hippocampal areas (J:109829)
• first observed plaques are fibrillar-core deposits; in 6 month old animals, diffuse plaques are apparent and these are abundant at 9 months, while in 9-12 month-old mice, plaques are visible in the thalamus (J:109829)
• no lesions are observed in the cerebellum or brain stem (J:109829)
• animals receiving no treatment display moderate amyloid pathology at 6 months, which progresses to a severe amyloid burden by 9 months (J:109829)
• mice raised for 6 months with no (DOX) treatment, followed by 3 or 6 months of DOX treatment show similar pathology to untreated 6-month old animals, despite relatively long lesion clearance times (J:109829)
• mice exhibit a progressive neuronal atrophy that is most pronounced in the granule cell layer of hippocampal dentate gyrus (J:185792)
• mice exhibit a progressive neuronal atrophy that is most pronounced in the granule cell layer of hippocampal dentate gyrus (J:185792)
• mice exhibit a progressive neuronal atrophy that is most pronounced in the granule cell layer of hippocampal dentate gyrus (J:185792)
• however, when mice are reared on doxycycline, cell loss is not observed (J:185792)
• mice exhibit a progressive neuronal atrophy that is most pronounced in the granule cell layer of hippocampal dentate gyrus (J:185792)
• however, when mice are reared on doxycycline, cell loss is not observed (J:185792)
• first visible plaques are fibrillary-cored deposits (J:109829)
• first visible plaques are fibrillary-cored deposits (J:109829)
• activated astrocytes are found near plaques in all affected mice glial pathology is more severe in older mice (J:109829)
• if transgene expression is suppressed with doxycycline treatment, pathology does not progress in severity (J:109829)
• activated astrocytes are found near plaques in all affected mice glial pathology is more severe in older mice (J:109829)
• if transgene expression is suppressed with doxycycline treatment, pathology does not progress in severity (J:109829)
• mice produce transgenic APP protein at 10- to 30-fold over endogenous App levels (J:109829)
• sensitivity of transgene suppression by doxycycline is intermediate between mice of line 885 and line 102 (J:109829)
• mice produce transgenic APP protein at 10- to 30-fold over endogenous App levels (J:109829)
• sensitivity of transgene suppression by doxycycline is intermediate between mice of line 885 and line 102 (J:109829)
• neuritic pathology is observed around plaques; neuritic pathology is more severe in older mice (J:109829)
• if transgene expression is suppressed with doxycycline treatment, pathology does not progress in severity (J:109829)
• neuritic pathology is observed around plaques; neuritic pathology is more severe in older mice (J:109829)
• if transgene expression is suppressed with doxycycline treatment, pathology does not progress in severity (J:109829)

behavior/neurological
• all animals raised with doxycycline have altered circadian rhythms with less distinction between day- and nighttime activity levels (J:109829)
• all animals raised with doxycycline have altered circadian rhythms with less distinction between day- and nighttime activity levels (J:109829)
• hyperactive behavior is partially reversed in some mice by 1 month of transgene suppression starting at 4-5 months of age (J:109829)
• hyperactive behavior is partially reversed in some mice by 1 month of transgene suppression starting at 4-5 months of age (J:109829)
• untreated mice show hyperactivity, often running in circles around the perimeter of cages (J:109829)
• similar patterns of activity are observed in Morris water maze, with repetitive swim patterns seen in radial water maze swim test (J:109829)
• hyperactive phenotype penetrance is ~100% (J:109829)
• untreated mice show 10-fold more ambulatory activity during the dark phase; even in light phase, activity is several-fold increased compared to wild-type controls; this activity is completely abolished in mice raised on doxycycline (J:109829)
• untreated mice show hyperactivity, often running in circles around the perimeter of cages (J:109829)
• similar patterns of activity are observed in Morris water maze, with repetitive swim patterns seen in radial water maze swim test (J:109829)
• hyperactive phenotype penetrance is ~100% (J:109829)
• untreated mice show 10-fold more ambulatory activity during the dark phase; even in light phase, activity is several-fold increased compared to wild-type controls; this activity is completely abolished in mice raised on doxycycline (J:109829)

immune system
• neuritic pathology is observed around plaques; neuritic pathology is more severe in older mice (J:109829)
• if transgene expression is suppressed with doxycycline treatment, pathology does not progress in severity (J:109829)
• neuritic pathology is observed around plaques; neuritic pathology is more severe in older mice (J:109829)
• if transgene expression is suppressed with doxycycline treatment, pathology does not progress in severity (J:109829)

homeostasis/metabolism
• doxycycline-mediated suppression of transgenic APPSwInd synthesis leads to parallel reductions of amyloid beta peptide levels (J:109829)
• early onset amyloid formation is observed, with plaques observed as early as 8 weeks of age in mice receiving no doxycycline (DOX) treatment (J:109829)
• plaques are restricted to the forebrain, including the cortex, hippocampus, olfactory bulb, and striatum; by 6 months, amyloid burden covers large cortical and hippocampal areas (J:109829)
• first observed plaques are fibrillar-core deposits; in 6 month old animals, diffuse plaques are apparent and these are abundant at 9 months, while in 9-12 month-old mice, plaques are visible in the thalamus (J:109829)
• no lesions are observed in the cerebellum or brain stem (J:109829)
• animals receiving no treatment display moderate amyloid pathology at 6 months, which progresses to a severe amyloid burden by 9 months (J:109829)
• mice raised for 6 months with no (DOX) treatment, followed by 3 or 6 months of DOX treatment show similar pathology to untreated 6-month old animals, despite relatively long lesion clearance times (J:109829)
• doxycycline-mediated suppression of transgenic APPSwInd synthesis leads to parallel reductions of amyloid beta peptide levels (J:109829)
• early onset amyloid formation is observed, with plaques observed as early as 8 weeks of age in mice receiving no doxycycline (DOX) treatment (J:109829)
• plaques are restricted to the forebrain, including the cortex, hippocampus, olfactory bulb, and striatum; by 6 months, amyloid burden covers large cortical and hippocampal areas (J:109829)
• first observed plaques are fibrillar-core deposits; in 6 month old animals, diffuse plaques are apparent and these are abundant at 9 months, while in 9-12 month-old mice, plaques are visible in the thalamus (J:109829)
• no lesions are observed in the cerebellum or brain stem (J:109829)
• animals receiving no treatment display moderate amyloid pathology at 6 months, which progresses to a severe amyloid burden by 9 months (J:109829)
• mice raised for 6 months with no (DOX) treatment, followed by 3 or 6 months of DOX treatment show similar pathology to untreated 6-month old animals, despite relatively long lesion clearance times (J:109829)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:109829


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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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last database update
02/02/2016
MGI 6.02
The Jackson Laboratory