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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Gfap-TGFB1)64Lms
transgene insertion 64, Lennart Mucke
MGI:3717676
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cx1
Tg(Gfap-TGFB1)64Lms/0
Tg(PDGFB-APPSwInd)20Lms/0
involves: BALB/c * C57BL/6 * DBA/2 * SJL MGI:4882081
cx2
Tg(Gfap-TGFB1)64Lms/0
Tg(PDGFB-APPInd)H6Lms/0
involves: BALB/c * SJL MGI:3717712
tg3
Tg(Gfap-TGFB1)64Lms/Tg(Gfap-TGFB1)64Lms involves: BALB/c * SJL MGI:3717707
tg4
Tg(Gfap-TGFB1)64Lms/0 involves: BALB/c * SJL MGI:3717708


Genotype
MGI:4882081
cx1
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:3717712
cx2
Allelic
Composition
Tg(Gfap-TGFB1)64Lms/0
Tg(PDGFB-APPInd)H6Lms/0
Genetic
Background
involves: BALB/c * 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
nervous system
• double transgenic mice display cerebrovascular deposits by 2-3 months of age, while single transgenic littermates have no such deposits at that age (J:102272)
• double transgenic mice display cerebrovascular deposits by 2-3 months of age, while single transgenic littermates have no such deposits at that age (J:102272)

homeostasis/metabolism
• double transgenic mice display cerebrovascular and meningeal amyloid deposits by 2-3 months of age, while single transgenic littermates have no such deposits at that age (J:102272)
• double transgenic mice display cerebrovascular and meningeal amyloid deposits by 2-3 months of age, while single transgenic littermates have no such deposits at that age (J:102272)
• double transgenic mice display cerebrovascular deposits by 2-3 months of age, while single transgenic littermates have no such deposits at that age (J:102272)
• double transgenic mice display cerebrovascular deposits by 2-3 months of age, while single transgenic littermates have no such deposits at that age (J:102272)




Genotype
MGI:3717707
tg3
Allelic
Composition
Tg(Gfap-TGFB1)64Lms/Tg(Gfap-TGFB1)64Lms
Genetic
Background
involves: BALB/c * 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
growth/size/body
• at 23 days of age, animals are dwarfs with reduced body weights (6.7 grams) compared to heterozygous or non-transgenic littermates (11.1 grams) (J:27781)
• at 23 days of age, animals are dwarfs with reduced body weights (6.7 grams) compared to heterozygous or non-transgenic littermates (11.1 grams) (J:27781)

behavior/neurological
• hydroencephaly is accompanied by development of tremors (J:27781)
• hydroencephaly is accompanied by development of tremors (J:27781)
• hydroencephaly is accompanied by lack of coordination (J:27781)
• hydroencephaly is accompanied by lack of coordination (J:27781)
• hydroencephaly is accompanied by hunched posture (J:27781)
• hydroencephaly is accompanied by hunched posture (J:27781)
• hydroencephaly is accompanied by development of seizures (J:27781)
• hydroencephaly is accompanied by development of seizures (J:27781)

nervous system
• hydroencephaly is accompanied by development of seizures (J:27781)
• hydroencephaly is accompanied by development of seizures (J:27781)
• between 7 and 20 days after birth, all mice develop hydroencephaly (J:27781)
• between 7 and 20 days after birth, all mice develop hydroencephaly (J:27781)
• lateral, third, and fourth ventricles are grossly enlarged; ependymal canal is severely enlarged (J:27781)
• foramina through which cerebrospinal fluid circulates remain open (J:27781)
• lateral, third, and fourth ventricles are grossly enlarged; ependymal canal is severely enlarged (J:27781)
• foramina through which cerebrospinal fluid circulates remain open (J:27781)
• sylvian canal is enlarged (J:27781)
• sylvian canal is enlarged (J:27781)
• brain regions adjacent to dilated cerebrospinal fluid spaces exhibit atrophy by compression (J:27781)
• brain regions adjacent to dilated cerebrospinal fluid spaces exhibit atrophy by compression (J:27781)
• mice show characteristic pattern of perivascular astrocytosis (J:27781)
• mice show characteristic pattern of perivascular astrocytosis (J:27781)
• meningeal coverings are thicker than in hemizygotes or controls (J:27781)
• meningeal coverings are thicker than in hemizygotes or controls (J:27781)

immune system
N
• no inflammatory cell infiltrates are seen in control mice or in transgenic mice displaying hydroencephaly (J:27781)
• no inflammatory cell infiltrates are seen in control mice or in transgenic mice displaying hydroencephaly (J:27781)




Genotype
MGI:3717708
tg4
Allelic
Composition
Tg(Gfap-TGFB1)64Lms/0
Genetic
Background
involves: BALB/c * 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
nervous system
• in 12-18 month old mice, prominent amyloid deposits are observed in cerebral blood vessels, whereas none are seen in controls (J:102272)
• in 12-18 month old mice, prominent amyloid deposits are observed in cerebral blood vessels, whereas none are seen in controls (J:102272)
• hydroencephaly was observed in only 1% (1/101) of hemizygous mice (J:27781)
• hydroencephaly was observed in only 1% (1/101) of hemizygous mice (J:27781)
• mice show characteristic pattern of perivascular astrocytosis, that is less intense than in homozygotes (J:27781)
• mice show characteristic pattern of perivascular astrocytosis, that is less intense than in homozygotes (J:27781)
• meningeal coverings are thicker than controls (J:27781)
• meningeal coverings are thicker than controls (J:27781)
• astrocytes secrete increased amounts of bioactive TGF-B1 (J:27781)
• astrocytes secrete increased amounts of bioactive TGF-B1 (J:27781)

immune system
N
• no inflammatory cell infiltrates are seen in hemizygous or control mice (J:27781)
• no inflammatory cell infiltrates are seen in hemizygous or control mice (J:27781)

homeostasis/metabolism
• in 12-18 month old mice, prominent amyloid deposits are observed in meninges, whereas none are seen in controls (J:102272)
• in 12-18 month old mice, prominent amyloid deposits are observed in meninges, whereas none are seen in controls (J:102272)
• in 12-18 month old mice, prominent amyloid deposits are observed in cerebral blood vessels, whereas none are seen in controls (J:102272)
• in 12-18 month old mice, prominent amyloid deposits are observed in cerebral blood vessels, whereas none are seen in controls (J:102272)





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