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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 15 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cx1
Psen1tm4.1Shn/Psen1+
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129 * C57BL/6 * C57BL/6J * DBA/2 MGI:5754381
cx2
Apoetm1Unc/Apoetm3(APOE_i4)Yhg
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 MGI:5427502
cx3
Apoetm1Unc/Apoetm2(APOE_i3)Yhg
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2 MGI:5427501
cx4
C3tm1Crr/C3tm1Crr
Tg(PDGFB-APPSwInd)20Lms/?
involves: 129S4/SvJae * C57BL/6 MGI:5295993
cx5
Pla2g4atm1Jvb/Pla2g4atm1Jvb
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4358900
cx6
Pla2g4atm1Jvb/Pla2g4a+
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4358899
cx7
Mapttm1Hnd/Mapt+
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:3718361
cx8
Mapttm1Hnd/Mapttm1Hnd
Tg(PDGFB-APPSwInd)20Lms/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:3718360
cx9
Tg(Gfap-TGFB1)64Lms/0
Tg(PDGFB-APPSwInd)20Lms/0
involves: BALB/c * C57BL/6 * DBA/2 * SJL MGI:4882081
cx10
Tg(Camk2a-tTA)1Mmay/0
Tg(PDGFB-APPSwInd)20Lms/0
Tg(tetO-MAPT)32Lms/0
involves: C57BL/6 * C57BL/6J * DBA/2 MGI:5828494
cx11
Tg(Camk2a-tTA)1Mmay/0
Tg(PDGFB-APPSwInd)20Lms/0
Tg(tetO-MAPT*A152T)L1Lms/0
involves: C57BL/6 * C57BL/6J * DBA/2 MGI:5828493
cx12
Tg(Camk2a-IDE)1Selk/0
Tg(PDGFB-APPSwInd)20Lms/0
involves: C57BL/6 * DBA/2 MGI:3721976
cx13
Tg(Camk2a-MME)3Selk/0
Tg(PDGFB-APPSwInd)20Lms/0
involves: C57BL/6 * DBA/2 MGI:3721977
tg14
Tg(PDGFB-APPSwInd)20Lms/0 B6.Cg-Tg(PDGFB-APPSwInd)20Lms MGI:3784691
tg15
Tg(PDGFB-APPSwInd)20Lms/0 involves: C57BL/6 * DBA/2 MGI:3639711


Genotype
MGI:5754381
cx1
Allelic
Composition
Psen1tm4.1Shn/Psen1+
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Psen1tm4.1Shn mutation (0 available); any Psen1 mutation (34 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• accelerated amyloid deposition in the cerebral cortex at 9 months of age compared to single Tg(PDGFB-APPSwInd)20Lms hemizygotes

nervous system
• accelerated amyloid deposition in the cerebral cortex at 9 months of age compared to single Tg(PDGFB-APPSwInd)20Lms hemizygotes




Genotype
MGI:5427502
cx2
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 (23 available); any Apoe mutation (80 available)
Apoetm3(APOE_i4)Yhg mutation (0 available); any Apoe mutation (80 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 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

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




Genotype
MGI:5427501
cx3
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 (23 available); any Apoe mutation (80 available)
Apoetm2(APOE_i3)Yhg mutation (0 available); any Apoe mutation (80 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 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

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




Genotype
MGI:5295993
cx4
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 (48 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• 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
• neuron loss in the CA3 region at 17 days relative to controls

immune system

hematopoietic system

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
• plasma amyloid levels are increased 51% at 17 months




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 (18 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 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

behavior/neurological
N
• mice do not exhibit the hyperactivity observed in Tg(PDGFB-APPSwInd)20Lms mice
• 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
• 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




Genotype
MGI:4358899
cx6
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 (18 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 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

behavior/neurological
N
• mice do not exhibit the hyperactivity observed in Tg(PDGFB-APPSwInd)20Lms mice
• 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
• 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




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 (408 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice show no signs of hyperactivity
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt
• 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

nervous system
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt
• 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
• mice show neuritic dystrophy around amyloid plaques
• aberrant sprouting of hippocampal axons is observed in transgenic mice

cellular
• aberrant sprouting of hippocampal axons is observed in transgenic mice

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




Genotype
MGI:3718360
cx8
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 (408 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 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
• mice show no signs of hyperactivity
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt

nervous system
• seizures are less severe and occur at longer latencies compared to transgenic mice with wild-type Mapt
• 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
• mice show neuritic dystrophy around amyloid plaques
• aberrant sprouting of hippocampal axons is observed in transgenic mice

cellular
• aberrant sprouting of hippocampal axons is observed in transgenic mice

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




Genotype
MGI:4882081
cx9
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)
Mouse lines carrying:
Tg(Gfap-TGFB1)64Lms mutation (1 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 available)
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
• 12- and 18-month old mutants show impaired probe trial performance, indicating a memory impairment

cardiovascular system
• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels
• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness
• 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

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
• 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

nervous system
• mutants exhibit significant collagen accumulation in penetrating intraparenchymal microvessels and in the surface pial membrane, resulting in increased thickness
• 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
• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels
• mutants exhibit activated GFAP-positive astrocytes in the cortex; activated astrocytes are distributed in clusters as well as diffusely throughout the cortex
• mutants exhibit significant collagen accumulation in the surface pial membrane, resulting in increased thickness
• about 22-23% reduction in the number of cortical cholinergic fibers in adults and aged-mutants
• 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

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
• 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
• 18 month old mutants exhibit widespread cerebral amyloid angiopathy in pial, intracortical, and hippocampal brain vessels

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Alzheimer's disease DOID:10652 OMIM:104300
OMIM:502500
OMIM:604154
OMIM:608907
J:167619




Genotype
MGI:5828494
cx10
Allelic
Composition
Tg(Camk2a-tTA)1Mmay/0
Tg(PDGFB-APPSwInd)20Lms/0
Tg(tetO-MAPT)32Lms/0
Genetic
Background
involves: C57BL/6 * C57BL/6J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Camk2a-tTA)1Mmay mutation (8 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 available)
Tg(tetO-MAPT)32Lms mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• fewer than the expected numbers (only 5 of 94) of mice were obtained, indicating a trend toward early lethality
• 2 of 5 surviving mice die at 2 months of age




Genotype
MGI:5828493
cx11
Allelic
Composition
Tg(Camk2a-tTA)1Mmay/0
Tg(PDGFB-APPSwInd)20Lms/0
Tg(tetO-MAPT*A152T)L1Lms/0
Genetic
Background
involves: C57BL/6 * C57BL/6J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Camk2a-tTA)1Mmay mutation (8 available)
Tg(PDGFB-APPSwInd)20Lms mutation (1 available)
Tg(tetO-MAPT*A152T)L1Lms mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• surviving mice die shortly after weaning
• fewer than the expected numbers (only 2 of 141) of mice were obtained, indicating early lethality




Genotype
MGI:3721976
cx12
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 (1 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

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%
• microgliosis is reduced
• decreased relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates
• number of dystrophic neurites is reduced relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice

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%




Genotype
MGI:3721977
cx13
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 (1 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

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
• microgliosis is reduced
• decreased relative to Tg(PDGFB-APPSwInd)20Lms single transgenic littermates
• number of dystrophic neurites is reduced relative to Tg(PDGFB-APPSwInd)20Lms single transgenic mice

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




Genotype
MGI:3784691
tg14
Allelic
Composition
Tg(PDGFB-APPSwInd)20Lms/0
Genetic
Background
B6.Cg-Tg(PDGFB-APPSwInd)20Lms
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(PDGFB-APPSwInd)20Lms mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice develop amyloid peptide deposits by 5-7 months of age
• 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
• dystrophic neurites are associated with plaques

homeostasis/metabolism
• mice develop amyloid peptide deposits by 5-7 months of age




Genotype
MGI:3639711
tg15
Allelic
Composition
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(PDGFB-APPSwInd)20Lms mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 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)

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
• 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
• 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)
• mice exhibit disinhibition-like behaviors in an elevated plus maze compared with wild-type mice
• 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
• 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)
• mice show neuritic dystrophy around amyloid plaques
• aberrant sprouting of hippocampal axons is observed in transgenic mice
• neurodegeneration is indicated by an age dependent decrease in density of synaptophysin-immunoreactive presynaptic terminals

cellular
• aberrant sprouting of hippocampal axons is observed in transgenic mice

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)
• 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)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
Alzheimer's disease DOID:10652 OMIM:104300
OMIM:502500
OMIM:604154
OMIM:608907
J:62290





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last database update
09/12/2017
MGI 6.10
The Jackson Laboratory