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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(PDGFB-APPSwInd)20Lms
transgene insertion 20, Lennart Mucke
MGI:3057148
Summary 12 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cx1
Apoetm1Unc/Apoetm3(APOE_i4)Yhg
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 MGI:5427502
cx2
Apoetm1Unc/Apoetm2(APOE_i3)Yhg
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 MGI:5427501
cx3
C3tm1Crr/C3tm1Crr
Tg(PDGFB-APPSwInd)20Lms/?
involves: 129S4/SvJae * C57BL/6 MGI:5295993
cx4
Pla2g4atm1Jvb/Pla2g4a+
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4358899
cx5
Pla2g4atm1Jvb/Pla2g4atm1Jvb
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4358900
cx6
Mapttm1Hnd/Mapttm1Hnd
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:3718360
cx7
Mapttm1Hnd/Mapt+
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:3718361
cx8
Tg(Gfap-TGFB1)64Lms/0
Tg(PDGFB-APPSwInd)20Lms/0
involves: BALB/c * C57BL/6 * DBA/2 * SJL MGI:4882081
cx9
Tg(Camk2a-IDE)1Selk/0
Tg(PDGFB-APPSwInd)20Lms/0
involves: C57BL/6 * DBA/2 MGI:3721976
cx10
Tg(Camk2a-MME)3Selk/0
Tg(PDGFB-APPSwInd)20Lms/0
involves: C57BL/6 * DBA/2 MGI:3721977
tg11
Tg(PDGFB-APPSwInd)20Lms/0 B6.Cg-Tg(PDGFB-APPSwInd)20Lms MGI:3784691
tg12
Tg(PDGFB-APPSwInd)20Lms/0 involves: C57BL/6 * DBA/2 MGI:3639711


Genotype
MGI:5427502
cx1
Allelic
Composition
Apoetm1Unc/Apoetm3(APOE_i4)Yhg
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Apoetm3(APOE_i4)Yhg mutation (0 available); any Apoe mutation (64 available)
Tg(PDGFB-APPSwInd)20Lms mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• aged mice exhibit reduced amyloid plaques compared to Apoetm3(APOE_i4)Yhg/Apoetm3(APOE_i4)Yhg Tg(PDGFB-APPSwInd)20Lms mice (J:184138)
• aged mice exhibit reduced amyloid plaques compared to Apoetm3(APOE_i4)Yhg/Apoetm3(APOE_i4)Yhg Tg(PDGFB-APPSwInd)20Lms mice (J:184138)

homeostasis/metabolism
• aged mice exhibit reduced amyloid plaques compared to Apoetm3(APOE_i4)Yhg/Apoetm3(APOE_i4)Yhg Tg(PDGFB-APPSwInd)20Lms mice (J:184138)
• aged mice exhibit reduced amyloid plaques compared to Apoetm3(APOE_i4)Yhg/Apoetm3(APOE_i4)Yhg Tg(PDGFB-APPSwInd)20Lms mice (J:184138)




Genotype
MGI:5427501
cx2
Allelic
Composition
Apoetm1Unc/Apoetm2(APOE_i3)Yhg
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm1Unc mutation (22 available); any Apoe mutation (64 available)
Apoetm2(APOE_i3)Yhg mutation (0 available); any Apoe mutation (64 available)
Tg(PDGFB-APPSwInd)20Lms mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• aged mice exhibit reduced amyloid plaques compared to Apoetm2(APOE_i3)Yhg/Apoetm2(APOE_i3)Yhg Tg(PDGFB-APPSwInd)20Lms mice (J:184138)
• aged mice exhibit reduced amyloid plaques compared to Apoetm2(APOE_i3)Yhg/Apoetm2(APOE_i3)Yhg Tg(PDGFB-APPSwInd)20Lms mice (J:184138)

homeostasis/metabolism
• aged mice exhibit reduced amyloid plaques compared to Apoetm2(APOE_i3)Yhg/Apoetm2(APOE_i3)Yhg Tg(PDGFB-APPSwInd)20Lms mice (J:184138)
• aged mice exhibit reduced amyloid plaques compared to Apoetm2(APOE_i3)Yhg/Apoetm2(APOE_i3)Yhg Tg(PDGFB-APPSwInd)20Lms mice (J:184138)




Genotype
MGI:5295993
cx3
Allelic
Composition
C3tm1Crr/C3tm1Crr
Tg(PDGFB-APPSwInd)20Lms/?
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
C3tm1Crr mutation (2 available); any C3 mutation (8 available)
Tg(PDGFB-APPSwInd)20Lms mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• increased (J:135902)
• increased (J:135902)
• plaque levels are doubled in the hippocampus and mid frontal cortex relative to controls at 17 months of age but normal at 12 months (J:135902)
• plasma amyloid levels are increased 51% at 17 months (J:135902)
• plaque levels are doubled in the hippocampus and mid frontal cortex relative to controls at 17 months of age but normal at 12 months (J:135902)
• plasma amyloid levels are increased 51% at 17 months (J:135902)
• neuron loss in the CA3 region at 17 days relative to controls (J:135902)
• neuron loss in the CA3 region at 17 days relative to controls (J:135902)

immune system
• increased (J:135902)
• increased (J:135902)

hematopoietic system
• increased (J:135902)
• increased (J:135902)

homeostasis/metabolism
• plaque levels are doubled in the hippocampus and mid frontal cortex relative to controls at 17 months of age but normal at 12 months (J:135902)
• plasma amyloid levels are increased 51% at 17 months (J:135902)
• plaque levels are doubled in the hippocampus and mid frontal cortex relative to controls at 17 months of age but normal at 12 months (J:135902)
• plasma amyloid levels are increased 51% at 17 months (J:135902)




Genotype
MGI:4358899
cx4
Allelic
Composition
Pla2g4atm1Jvb/Pla2g4a+
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pla2g4atm1Jvb mutation (0 available); any Pla2g4a mutation (2 available)
Tg(PDGFB-APPSwInd)20Lms mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice do not exhibit premature death as do Tg(PDGFB-APPSwInd)20Lms mice (J:141084)
• mice do not exhibit premature death as do Tg(PDGFB-APPSwInd)20Lms mice (J:141084)

behavior/neurological
N
• mice do not exhibit the hyperactivity observed in Tg(PDGFB-APPSwInd)20Lms mice (J:141084)
• mice do not exhibit the hyperactivity observed in Tg(PDGFB-APPSwInd)20Lms mice (J:141084)
• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice that are not as severe as in Tg(PDGFB-APPSwInd)20Lms mice (J:141084)
• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice that are not as severe as in Tg(PDGFB-APPSwInd)20Lms mice (J:141084)
• mice exhibit a complete or partial recovery of the learning deficits observed in Tg(PDGFB-APPSwInd)20Lms mice with improved target crossing in a Morris water maze (J:141084)
• mice exhibit a complete or partial recovery of the learning deficits observed in Tg(PDGFB-APPSwInd)20Lms mice with improved target crossing in a Morris water maze (J:141084)




Genotype
MGI:4358900
cx5
Allelic
Composition
Pla2g4atm1Jvb/Pla2g4atm1Jvb
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pla2g4atm1Jvb mutation (0 available); any Pla2g4a mutation (2 available)
Tg(PDGFB-APPSwInd)20Lms mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice do not exhibit premature death as do Tg(PDGFB-APPSwInd)20Lms mice (J:141084)
• mice do not exhibit premature death as do Tg(PDGFB-APPSwInd)20Lms mice (J:141084)

behavior/neurological
N
• mice do not exhibit the hyperactivity observed in Tg(PDGFB-APPSwInd)20Lms mice (J:141084)
• mice do not exhibit the hyperactivity observed in Tg(PDGFB-APPSwInd)20Lms mice (J:141084)
• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice that are not as severe as in Tg(PDGFB-APPSwInd)20Lms mice (J:141084)
• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice that are not as severe as in Tg(PDGFB-APPSwInd)20Lms mice (J:141084)
• mice exhibit a complete or partial recovery of the learning deficits observed in Tg(PDGFB-APPSwInd)20Lms mice with improved target crossing in a Morris water maze (J:141084)
• mice exhibit a complete or partial recovery of the learning deficits observed in Tg(PDGFB-APPSwInd)20Lms mice with improved target crossing in a Morris water maze (J:141084)




Genotype
MGI:3718360
cx6
Allelic
Composition
Mapttm1Hnd/Mapttm1Hnd
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapttm1Hnd mutation (7 available); any Mapt mutation (393 available)
Tg(PDGFB-APPSwInd)20Lms mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice show normal spatial learning and object-recongition memory, at levels similar to non-transgenic controls (J:121330)
• mice show no signs of hyperactivity (J:121330)
• mice show normal spatial learning and object-recongition memory, at levels similar to non-transgenic controls (J:121330)
• mice show no signs of hyperactivity (J:121330)
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt (J:121330)
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt (J:121330)

nervous system
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt (J:121330)
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt (J:121330)
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous or wild-type for Mapt (J:121330)
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous or wild-type for Mapt (J:121330)
• mice show neuritic dystrophy around amyloid plaques (J:121330)
• mice show neuritic dystrophy around amyloid plaques (J:121330)
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)

cellular
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)

homeostasis/metabolism
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous or wild-type for Mapt (J:121330)
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous or wild-type for Mapt (J:121330)




Genotype
MGI:3718361
cx7
Allelic
Composition
Mapttm1Hnd/Mapt+
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Mapttm1Hnd mutation (7 available); any Mapt mutation (393 available)
Tg(PDGFB-APPSwInd)20Lms mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice show no signs of hyperactivity (J:121330)
• mice show no signs of hyperactivity (J:121330)
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt (J:121330)
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt (J:121330)
• in the hidden platform version of the Morris water maze, non-trangenic controls, regardless of Mapt genotype learn the task over 3 days, whereas transgenic mice heterozygous for Mapttm1Hnd show show impaired learning compared to controls but less impairment than transgenic mice with normal Mapt expression (J:121330)
• in probe trials where the platform is removed, mice show delayed learning, compared to non transgenic controls or transgenic mice with wild-type Mapt, with more target than non-target crossings after 5 days of training (J:121330)
• in the hidden platform version of the Morris water maze, non-trangenic controls, regardless of Mapt genotype learn the task over 3 days, whereas transgenic mice heterozygous for Mapttm1Hnd show show impaired learning compared to controls but less impairment than transgenic mice with normal Mapt expression (J:121330)
• in probe trials where the platform is removed, mice show delayed learning, compared to non transgenic controls or transgenic mice with wild-type Mapt, with more target than non-target crossings after 5 days of training (J:121330)

nervous system
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt (J:121330)
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt (J:121330)
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics null or wild-type for Mapt (J:121330)
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics null or wild-type for Mapt (J:121330)
• mice show neuritic dystrophy around amyloid plaques (J:121330)
• mice show neuritic dystrophy around amyloid plaques (J:121330)
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)

cellular
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)

homeostasis/metabolism
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics null or wild-type for Mapt (J:121330)
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics null or wild-type for Mapt (J:121330)




Genotype
MGI:4882081
cx8
Allelic
Composition
Tg(Gfap-TGFB1)64Lms/0
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: BALB/c * C57BL/6 * DBA/2 * SJL
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
• 6-8 month old mutants show increased latencies to locate the hidden platform in the Morris water maze indicating a learning deficit (J:167619)
• 6-8 month old mutants show increased latencies to locate the hidden platform in the Morris water maze indicating a learning deficit (J:167619)
• 12- and 18-month old mutants show impaired probe trial performance, indicating a memory impairment (J:167619)
• 12- and 18-month old mutants show impaired probe trial performance, indicating a memory impairment (J:167619)

cardiovascular system
• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels (J:167619)
• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels (J:167619)
• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness (J:167619)
• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness (J:167619)
• 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 (J:167619)
• arterial dysfunction is not due to oxidative stress (J:167619)
• by 18 months of age, mutants exhibit impaired maximal diameter decrease during NOS inhibition with N-nitro-L-arginine (J:167619)
• however, contractile response of arteries to endothelin-1 is normal (J:167619)
• 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 (J:167619)
• arterial dysfunction is not due to oxidative stress (J:167619)
• by 18 months of age, mutants exhibit impaired maximal diameter decrease during NOS inhibition with N-nitro-L-arginine (J:167619)
• however, contractile response of arteries to endothelin-1 is normal (J:167619)

muscle
• 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 (J:167619)
• arterial dysfunction is not due to oxidative stress (J:167619)
• by 18 months of age, mutants exhibit impaired maximal diameter decrease during NOS inhibition with N-nitro-L-arginine (J:167619)
• however, contractile response of arteries to endothelin-1 is normal (J:167619)
• 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 (J:167619)
• arterial dysfunction is not due to oxidative stress (J:167619)
• by 18 months of age, mutants exhibit impaired maximal diameter decrease during NOS inhibition with N-nitro-L-arginine (J:167619)
• however, contractile response of arteries to endothelin-1 is normal (J:167619)

nervous system
• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness (J:167619)
• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness (J:167619)
• mutants exhibit age-dependent amyloid beta plaque deposition in the cortex and hippocampus; 18 month old mutants exhibit parenchymal amyloid beta senile plaques (J:167619)
• 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 (J:167619)
• mutants exhibit age-dependent amyloid beta plaque deposition in the cortex and hippocampus; 18 month old mutants exhibit parenchymal amyloid beta senile plaques (J:167619)
• 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 (J:167619)
• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels (J:167619)
• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels (J:167619)
• mutants exhibit activated GFAP-positive astrocytes in the cortex; activated astrocytes are distributed in clusters as well as diffusely throughout the cortex (J:167619)
• mutants exhibit activated GFAP-positive astrocytes in the cortex; activated astrocytes are distributed in clusters as well as diffusely throughout the cortex (J:167619)
• mutants exhibit significant collagen accumulation in the surface pial membrane, resulting in increased thickness (J:167619)
• mutants exhibit significant collagen accumulation in the surface pial membrane, resulting in increased thickness (J:167619)
• about 22-23% reduction in the number of cortical cholinergic fibers in adults and aged-mutants (J:167619)
• about 22-23% reduction in the number of cortical cholinergic fibers in adults and aged-mutants (J:167619)
• glucose uptake is impaired in activated somatosensory cortex of aged mutants after whisker stimulation (J:167619)
• gradual loss of the neuronally-driven hemodynamic response to sensory whisker stimulation (J:167619)
• glucose uptake is impaired in activated somatosensory cortex of aged mutants after whisker stimulation (J:167619)
• gradual loss of the neuronally-driven hemodynamic response to sensory whisker stimulation (J:167619)

homeostasis/metabolism
• mutants exhibit age-dependent amyloid beta plaque deposition in the cortex and hippocampus; 18 month old mutants exhibit parenchymal amyloid beta senile plaques (J:167619)
• 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 (J:167619)
• mutants exhibit age-dependent amyloid beta plaque deposition in the cortex and hippocampus; 18 month old mutants exhibit parenchymal amyloid beta senile plaques (J:167619)
• 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 (J:167619)
• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels (J:167619)
• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels (J:167619)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:167619




Genotype
MGI:3721976
cx9
Allelic
Composition
Tg(Camk2a-IDE)1Selk/0
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Camk2a-IDE)1Selk mutation (1 available)
Tg(PDGFB-APPSwInd)20Lms mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• attenuated premature death at 6 months relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates (J:87150)
• attenuated premature death at 6 months relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates (J:87150)

nervous system
• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~50% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaque burden is reduced by ~50% (J:87150)
• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~50% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaque burden is reduced by ~50% (J:87150)
• microgliosis is reduced (J:87150)
• microgliosis is reduced (J:87150)
• decreased relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates (J:87150)
• decreased relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates (J:87150)
• number of dystrophic neurites is reduced relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice (J:87150)
• number of dystrophic neurites is reduced relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice (J:87150)

homeostasis/metabolism
• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~50% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaque burden is reduced by ~50% (J:87150)
• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~50% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaque burden is reduced by ~50% (J:87150)




Genotype
MGI:3721977
cx10
Allelic
Composition
Tg(Camk2a-MME)3Selk/0
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Camk2a-MME)3Selk mutation (1 available)
Tg(PDGFB-APPSwInd)20Lms mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• attenuated premature death at 6 months relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates (J:87150)
• attenuated premature death at 6 months relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates (J:87150)

nervous system
• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~90% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaques are almost absent (J:87150)
• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~90% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaques are almost absent (J:87150)
• microgliosis is reduced (J:87150)
• microgliosis is reduced (J:87150)
• decreased relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates (J:87150)
• decreased relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates (J:87150)
• number of dystrophic neurites is reduced relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice (J:87150)
• number of dystrophic neurites is reduced relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice (J:87150)

homeostasis/metabolism
• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~90% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaques are almost absent (J:87150)
• at 6-10 months, soluble and insoluble Abeta-40 and -42 peptide levels are reduced by ~90% relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice; amyloid plaques are almost absent (J:87150)




Genotype
MGI:3784691
tg11
Allelic
Composition
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
B6.Cg-Tg(PDGFB-APPSwInd)20Lms
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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
• mice develop amyloid peptide deposits by 5-7 months of age (J:100954)
• mice develop amyloid peptide deposits by 5-7 months of age (J:100954)
• at 6 months and 12 to 16 months of age, 30% fewer pyramidal cells in the entorhinal cortex express Reelin than in wild-type mice (J:118589)
• however, no neuron loss is observed (J:118589)
• at 6 months and 12 to 16 months of age, 30% fewer pyramidal cells in the entorhinal cortex express Reelin than in wild-type mice (J:118589)
• however, no neuron loss is observed (J:118589)
• dystrophic neurites are associated with plaques (J:100954)
• dystrophic neurites are associated with plaques (J:100954)

homeostasis/metabolism
• mice develop amyloid peptide deposits by 5-7 months of age (J:100954)
• mice develop amyloid peptide deposits by 5-7 months of age (J:100954)




Genotype
MGI:3639711
tg12
Allelic
Composition
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: C57BL/6 * DBA/2
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
mortality/aging
• high rate of premature (6 months or earlier) death (J:87150)
• high rate of premature (6 months or earlier) death (J:87150)
• mice show premature death of unclear etiology with >15% mortality exhibited by 6 months, compared to all other genotypes (J:121330)
• mice show premature death of unclear etiology with >15% mortality exhibited by 6 months, compared to all other genotypes (J:121330)

behavior/neurological
• mice are abnormally sensitive to pentylenetetrazole (PTZ)-induced seizures with 20% suffering fatal status epilepticus at a PTZ dose not lethal in non-transgenic controls (J:121330)
• mice are abnormally sensitive to pentylenetetrazole (PTZ)-induced seizures with 20% suffering fatal status epilepticus at a PTZ dose not lethal in non-transgenic controls (J:121330)
• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice (J:141084)
• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice (J:141084)
• at 4-7 months of age, mice transgenic mice with wild-type Mapt expression take longer to locate the platform in the cued version of the Morris water maze test compared to transgenic mice heterozygous or homozygous for Mapt deletion (J:121330)
• at 4-7 months of age, mice transgenic mice with wild-type Mapt expression take longer to locate the platform in the cued version of the Morris water maze test compared to transgenic mice heterozygous or homozygous for Mapt deletion (J:121330)
• in the hidden platform version of the Morris water maze, non-trangenic controls, regardless of Mapt genotype learn the task over 3 days, whereas transgenic mice with wild-type expression of Mapt show no evidence of learning (J:121330)
• in probe trials where the platform is removed, mice show no learning, displaying no significantly elevated crossings of the target quadrant after 5 days of training (J:121330)
• in the hidden platform version of the Morris water maze, non-trangenic controls, regardless of Mapt genotype learn the task over 3 days, whereas transgenic mice with wild-type expression of Mapt show no evidence of learning (J:121330)
• in probe trials where the platform is removed, mice show no learning, displaying no significantly elevated crossings of the target quadrant after 5 days of training (J:121330)
• in a Morris water maze, mice fail to favor the target platform location unlike wild-type mice (J:141084)
• in a Morris water maze, mice fail to favor the target platform location unlike wild-type mice (J:141084)
• mice show hyperactivity in the Y-maze, a new cage, and elevated-plus maze compared to other transgenic mice or non-transgenic controls; this persists in mice 12-16 months of age (J:121330)
• mice show hyperactivity in the Y-maze, a new cage, and elevated-plus maze compared to other transgenic mice or non-transgenic controls; this persists in mice 12-16 months of age (J:121330)

nervous system
• mice are abnormally sensitive to pentylenetetrazole (PTZ)-induced seizures with 20% suffering fatal status epilepticus at a PTZ dose not lethal in non-transgenic controls (J:121330)
• mice are abnormally sensitive to pentylenetetrazole (PTZ)-induced seizures with 20% suffering fatal status epilepticus at a PTZ dose not lethal in non-transgenic controls (J:121330)
• diffuse immunoreactive amyloid deposits detected in dentate gyrus and neocortex of mice aged 5 to 7 months old (J:62290)
• all mice exhibit plaques by age 8 to 10 months (J:62290)
• diffuse immunoreactive amyloid deposits detected in dentate gyrus and neocortex of mice aged 5 to 7 months old (J:62290)
• all mice exhibit plaques by age 8 to 10 months (J:62290)
• soluble and insoluble Abeta-40 and -42 peptide deposits at 6-10 months (J:87150)
• soluble and insoluble Abeta-40 and -42 peptide deposits at 6-10 months (J:87150)
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous null for Mapt (J:121330)
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous null for Mapt (J:121330)
• mice show neuritic dystrophy around amyloid plaques (J:121330)
• mice show neuritic dystrophy around amyloid plaques (J:121330)
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)
• neurodegeneration is indicated by an age dependent decrease in density of synaptophysin-immunoreactive presynaptic terminals (J:62290)
• neurodegeneration is indicated by an age dependent decrease in density of synaptophysin-immunoreactive presynaptic terminals (J:62290)

cellular
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)
• aberrant sprouting of hippocampal axons is observed in transgenic mice (J:121330)

homeostasis/metabolism
• diffuse immunoreactive amyloid deposits detected in dentate gyrus and neocortex of mice aged 5 to 7 months old (J:62290)
• all mice exhibit plaques by age 8 to 10 months (J:62290)
• diffuse immunoreactive amyloid deposits detected in dentate gyrus and neocortex of mice aged 5 to 7 months old (J:62290)
• all mice exhibit plaques by age 8 to 10 months (J:62290)
• soluble and insoluble Abeta-40 and -42 peptide deposits at 6-10 months (J:87150)
• soluble and insoluble Abeta-40 and -42 peptide deposits at 6-10 months (J:87150)
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous null for Mapt (J:121330)
• at 4-7 months and 14-18 months, Abeta plaque deposition is observed, at levels the same as other transgenics heterozygous null for Mapt (J:121330)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:62290





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last database update
01/26/2016
MGI 6.02
The Jackson Laboratory