Analysis Tools|
Allele Symbol Allele Name Allele ID |
Zbtb20Tg(PDGFB-APPSwInd)20Lms transgene insertion 20, Lennart Mucke MGI:3057148 |
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| Summary |
16 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• accelerated amyloid deposition in the cerebral cortex at 9 months of age compared to single Tg(PDGFB-APPSwInd)20Lms hemizygotes
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• accelerated amyloid deposition in the cerebral cortex at 9 months of age compared to single Tg(PDGFB-APPSwInd)20Lms hemizygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• aged mice exhibit reduced amyloid plaques compared to Apoetm2(APOE_i3)Yhg/Apoetm2(APOE_i3)Yhg Tg(PDGFB-APPSwInd)20Lms mice
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• aged mice exhibit reduced amyloid plaques compared to Apoetm2(APOE_i3)Yhg/Apoetm2(APOE_i3)Yhg Tg(PDGFB-APPSwInd)20Lms mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• aged mice exhibit reduced amyloid plaques compared to Apoetm3(APOE_i4)Yhg/Apoetm3(APOE_i4)Yhg Tg(PDGFB-APPSwInd)20Lms mice
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• aged mice exhibit reduced amyloid plaques compared to Apoetm3(APOE_i4)Yhg/Apoetm3(APOE_i4)Yhg Tg(PDGFB-APPSwInd)20Lms mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• increased
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• plaque levels are doubled in the hippocampus and mid frontal cortex relative to controls at 17 months of age but normal at 12 months
• plasma amyloid levels are increased 51% at 17 months
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• neuron loss in the CA3 region at 17 days relative to controls
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• increased
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• increased
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• plaque levels are doubled in the hippocampus and mid frontal cortex relative to controls at 17 months of age but normal at 12 months
• plasma amyloid levels are increased 51% at 17 months
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice do not exhibit premature death as do Tg(PDGFB-APPSwInd)20Lms mice
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| N |
• mice do not exhibit the hyperactivity observed in Tg(PDGFB-APPSwInd)20Lms mice
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• 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
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice do not exhibit premature death as do Tg(PDGFB-APPSwInd)20Lms mice
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| N |
• mice do not exhibit the hyperactivity observed in Tg(PDGFB-APPSwInd)20Lms mice
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• 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
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice show normal spatial learning and object-recongition memory, at levels similar to non-transgenic controls
• mice show no signs of hyperactivity
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• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt
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• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt
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• 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
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• mice show neuritic dystrophy around amyloid plaques
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• aberrant sprouting of hippocampal axons is observed in transgenic mice
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• aberrant sprouting of hippocampal axons is observed in transgenic mice
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice show no signs of hyperactivity
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• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt
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• 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
• 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
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• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt
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• 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
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• mice show neuritic dystrophy around amyloid plaques
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• aberrant sprouting of hippocampal axons is observed in transgenic mice
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• aberrant sprouting of hippocampal axons is observed in transgenic mice
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 6-8 month old mutants show increased latencies to locate the hidden platform in the Morris water maze indicating a learning deficit
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• 12- and 18-month old mutants show impaired probe trial performance, indicating a memory impairment
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• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels
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• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness
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• 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
• arterial dysfunction is not due to oxidative stress
• by 18 months of age, mutants exhibit impaired maximal diameter decrease during NOS inhibition with N-nitro-L-arginine
• however, contractile response of arteries to endothelin-1 is normal
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• 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
• arterial dysfunction is not due to oxidative stress
• by 18 months of age, mutants exhibit impaired maximal diameter decrease during NOS inhibition with N-nitro-L-arginine
• however, contractile response of arteries to endothelin-1 is normal
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• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness
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• mutants exhibit age-dependent amyloid beta plaque deposition in the cortex and hippocampus; 18 month old mutants exhibit parenchymal amyloid beta senile plaques
• 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
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• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels
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• mutants exhibit activated GFAP-positive astrocytes in the cortex; activated astrocytes are distributed in clusters as well as diffusely throughout the cortex
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• mutants exhibit significant collagen accumulation in the surface pial membrane, resulting in increased thickness
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• about 22-23% reduction in the number of cortical cholinergic fibers in adults and aged-mutants
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• glucose uptake is impaired in activated somatosensory cortex of aged mutants after whisker stimulation
• gradual loss of the neuronally-driven hemodynamic response to sensory whisker stimulation
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• mutants exhibit age-dependent amyloid beta plaque deposition in the cortex and hippocampus; 18 month old mutants exhibit parenchymal amyloid beta senile plaques
• 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
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• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| Alzheimer's disease | DOID:10652 | J:167619 | ||
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• during the choice phase of the novel object recognition test, mice spend more time with the novel object and preference index shows that mice have greater preference toward the novel object indicating restoration of the recognition memory deficits seen in Zbtb20Tg(PDGFB-APPSwInd)20Lms/0 mice
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| N |
• hippocampal tissues show lower amyloid beta 40 and amyloid beta 42 levels than in Zbtb20Tg(PDGFB-APPSwInd)20Lms/0 mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• surviving mice die shortly after weaning
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• fewer than the expected numbers (only 2 of 141) of mice were obtained, indicating early lethality
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• fewer than the expected numbers (only 5 of 94) of mice were obtained, indicating a trend toward early lethality
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• 2 of 5 surviving mice die at 2 months of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• attenuated premature death at 6 months relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates
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• 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
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• decreased relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates
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• number of dystrophic neurites is reduced relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• attenuated premature death at 6 months relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates
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• 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%
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• decreased relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates
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• number of dystrophic neurites is reduced relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice
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• 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%
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• during the choice phase of the novel object recognition test, mice spend a similar amount of time exploring novel and old objects, indicating recognition memory deficits
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• mice develop amyloid peptide deposits by 5-7 months of age
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• 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
• however, no neuron loss is observed
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• dystrophic neurites are associated with plaques
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• mice develop amyloid peptide deposits by 5-7 months of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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)
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• 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
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• 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
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• 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)
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• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice
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• 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)
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• 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
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• 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)
• 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)
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• mice show neuritic dystrophy around amyloid plaques
|
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• aberrant sprouting of hippocampal axons is observed in transgenic mice
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• neurodegeneration is indicated by an age dependent decrease in density of synaptophysin-immunoreactive presynaptic terminals
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• aberrant sprouting of hippocampal axons is observed in transgenic mice
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• 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)
• 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)
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| Alzheimer's disease | DOID:10652 | J:62290 | ||
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 12/10/2024 MGI 6.24 |
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