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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(APPSWE)2576Kha
transgene insertion 2576, Karen Hsiao Ashe
MGI:2385631
Summary 34 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cx1
Pin1tm1Tuc/Pin1tm1Tuc
Tg(APPSWE)2576Kha/0
involves: 129 * 129P2/OlaHsd * C57BL/6 * SJL MGI:5433613
cx2
Psen1tm1Dgf/Psen1tm1Dgf
Tg(APPSWE)2576Kha/?
involves: 129 * C57BL/6 * CD-1 * SJL MGI:3611211
cx3
Nos2tm1Lau/Nos2tm1Lau
Tg(APPSWE)2576Kha/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:3769910
cx4
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae
Tg(APPSWE)2576Kha/?
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:4355224
cx5
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae
Tg(APPSWE)2576Kha/?
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:4355229
cx6
Vps35Gt(RRK261)Byg/Vps35+
Tg(APPSWE)2576Kha/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5306777
cx7
Psen1tm1Mpm/Psen1tm1Mpm
Tg(APPSWE)2576Kha/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL MGI:5292247
cx8
Psen1tm1Dgf/Psen1+
Tg(APPSWE)2576Kha/0
involves: 129S1/Sv * 129X1/SvJ * CD-1 * C57BL/6 * SJL MGI:2652383
cx9
Cd40lgtm1Flv/Cd40lgtm1Flv
Tg(APPSWE)2576Kha/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:2653196
cx10
Ccr2tm1Ifc/Ccr2+
Tg(APPSWE)2576Kha/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:4831171
cx11
Ccr2tm1Ifc/Ccr2tm1Ifc
Tg(APPSWE)2576Kha/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:4831169
cx12
Dab1tm1Bwh/Dab1tm1Bwh
Tg(APPSWE)2576Kha/0
involves: 129S4/SvJaeSor * C57BL/6 * SJL MGI:3810279
cx13
Appd1FVB/NCr/Appd1FVB/NCr
Tg(APPSWE)2576Kha/0
involves: 129S6/SvEvTac * C57BL/6 * FVB/NCr * SJL MGI:3663101
cx14
Appd2FVB/NCr/Appd2FVB/NCr
Tg(APPSWE)2576Kha/0
involves: 129S6/SvEvTac * C57BL/6 * FVB/NCr * SJL MGI:3663102
cx15
Psen1tm1Zhe/Psen1tm1Zhe
Tg(APPSWE)2576Kha/?
involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:3624416
cx16
Slc30a3tm1Rpa/Slc30a3tm1Rpa
Tg(APPSWE)2576Kha/0
involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:3029279
cx17
Ldlrtm1Her/Ldlrtm1Her
Tg(APPSWE)2576Kha/0
involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:4367205
cx18
Pld2tm1.1Gdp/Pld2+
Tg(APPSWE)2576Kha/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:4880015
cx19
Pld2tm1.1Gdp/Pld2tm1.1Gdp
Tg(APPSWE)2576Kha/0
involves: 129X1/SvJ * C57BL/6 * SJL MGI:4880014
cx20
Hspa4tm1.1Miv/Hspa4tm1.1Miv
Tg(APPSWE)2576Kha/0
involves: BALB/cJ * C57BL/6 * SJL MGI:4836978
cx21
Tg(APPSWE)2576Kha/0
Tg(Prnp-ITM2B/APP695*42)A12Emcg/0
involves: C3H * C57BL/6 * SJL MGI:3710765
cx22
Psen1tm1.1Tcs/Psen1tm1.1Tcs
Tg(APPSWE)2576Kha/0
involves: C57BL/6 * C57BL/6J * SJL MGI:5292246
cx23
Tg(APPSWE)2576Kha/0
Tg(PDGFB-PSEN1M146L)2Jhd/0
involves: C57BL/6 * DBA/2 * SJL MGI:3717259
cx24
Tg(APPSWE)2576Kha/0
Tg(Prnp-MAPT*P301L)JNPL3Hlmc/0
involves: C57BL/6 * DBA/2 * SJL * SW MGI:3720702
cx25
Tg(APPSWE)2576Kha/?
Tg(PDGFB-PSEN1M146L)2Jhd/?
involves: C57BL/6 * DBA/2 * SJL * SW MGI:3711709
cx26
Tg(APPSWE)2576Kha/0
Tg(PDGFB-PSEN1M146L)2Jhd/0
involves: C57BL/6 * DBA/2 * SJL * SW MGI:5140748
cx27
Tg(APPSWE)2576Kha/?
Tg(EIF1AX-Aldh2*E487K)101Oht/?
involves: C57BL/6 * SJL MGI:5699096
cx28
Tg(APPSWE)2576Kha/0
Tg(PSEN1)5Dbo/0
involves: C57BL/6 * SJL MGI:5463430
tg29
Tg(APPSWE)2576Kha/Tg(APPSWE)2576Kha involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:4366449
tg30
Tg(APPSWE)2576Kha/0 FVB.Cg-Tg(APPSWE)2576Kha MGI:3722308
tg31
Tg(APPSWE)2576Kha/0 involves: 129S7/SvEvBrd * C57BL/6 * SJL MGI:3029285
tg32
Tg(APPSWE)2576Kha/0 involves: C57BL/6 * DBA/2 * SJL * SW MGI:3720700
tg33
Tg(APPSWE)2576Kha/0 involves: C57BL/6J * SJL MGI:3722307
tg34
Tg(APPSWE)2576Kha/0 involves: C57BL/6 * SJL MGI:3710766


Genotype
MGI:5433613
cx1
Allelic
Composition
Pin1tm1Tuc/Pin1tm1Tuc
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129 * 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pin1tm1Tuc mutation (1 available); any Pin1 mutation (20 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• levels of insoluble amyloid beta, especially amyloid beta42, are increased by 46% at 6 months of age compared to single Tg(APPSWE)2576Kha hemizygous controls (J:107132)
• however, levels of soluble amyloid beta40 and amyloid beta42 are not affected (J:107132)
• amyloid beta42 predominately accumulates in multivesicular bodies of neurons (J:107132)
• levels of total APPs and beta-APPs are increased by about 3-fold, but levels of alpha-APPs are reduced by about 50% compared to single Tg(APPSWE)2576Kha hemizygous controls, indicating an increase in amyloidogenic versus non-amyloidogenic APP processing and thus elevation of the amyloid beta42 (J:107132)
• levels of insoluble amyloid beta, especially amyloid beta42, are increased by 46% at 6 months of age compared to single Tg(APPSWE)2576Kha hemizygous controls (J:107132)
• however, levels of soluble amyloid beta40 and amyloid beta42 are not affected (J:107132)
• amyloid beta42 predominately accumulates in multivesicular bodies of neurons (J:107132)
• levels of total APPs and beta-APPs are increased by about 3-fold, but levels of alpha-APPs are reduced by about 50% compared to single Tg(APPSWE)2576Kha hemizygous controls, indicating an increase in amyloidogenic versus non-amyloidogenic APP processing and thus elevation of the amyloid beta42 (J:107132)

homeostasis/metabolism
• levels of insoluble amyloid beta, especially amyloid beta42, are increased by 46% at 6 months of age compared to single Tg(APPSWE)2576Kha hemizygous controls (J:107132)
• however, levels of soluble amyloid beta40 and amyloid beta42 are not affected (J:107132)
• amyloid beta42 predominately accumulates in multivesicular bodies of neurons (J:107132)
• levels of total APPs and beta-APPs are increased by about 3-fold, but levels of alpha-APPs are reduced by about 50% compared to single Tg(APPSWE)2576Kha hemizygous controls, indicating an increase in amyloidogenic versus non-amyloidogenic APP processing and thus elevation of the amyloid beta42 (J:107132)
• levels of insoluble amyloid beta, especially amyloid beta42, are increased by 46% at 6 months of age compared to single Tg(APPSWE)2576Kha hemizygous controls (J:107132)
• however, levels of soluble amyloid beta40 and amyloid beta42 are not affected (J:107132)
• amyloid beta42 predominately accumulates in multivesicular bodies of neurons (J:107132)
• levels of total APPs and beta-APPs are increased by about 3-fold, but levels of alpha-APPs are reduced by about 50% compared to single Tg(APPSWE)2576Kha hemizygous controls, indicating an increase in amyloidogenic versus non-amyloidogenic APP processing and thus elevation of the amyloid beta42 (J:107132)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:107132




Genotype
MGI:3611211
cx2
Allelic
Composition
Psen1tm1Dgf/Psen1tm1Dgf
Tg(APPSWE)2576Kha/?
Genetic
Background
involves: 129 * C57BL/6 * CD-1 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Psen1tm1Dgf mutation (0 available); any Psen1 mutation (22 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• accelerated onset of amyloid deposition in a gene-dosage dependent manner (J:102425)
• amyloid-beta deposition was widely distributed throughout the brain and spinal cord (J:102425)
• accelerated onset of amyloid deposition in a gene-dosage dependent manner (J:102425)
• amyloid-beta deposition was widely distributed throughout the brain and spinal cord (J:102425)

homeostasis/metabolism
• accelerated onset of amyloid deposition in a gene-dosage dependent manner (J:102425)
• amyloid-beta deposition was widely distributed throughout the brain and spinal cord (J:102425)
• accelerated onset of amyloid deposition in a gene-dosage dependent manner (J:102425)
• amyloid-beta deposition was widely distributed throughout the brain and spinal cord (J:102425)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:102425




Genotype
MGI:3769910
cx3
Allelic
Composition
Nos2tm1Lau/Nos2tm1Lau
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nos2tm1Lau mutation (6 available); any Nos2 mutation (12 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• plaque levels elevated in the brain relative to control mice carrying the transgene only (J:112919)
• plaque levels elevated in the brain relative to control mice carrying the transgene only (J:112919)
• deposits are observed by 52 weeks of age (J:143551)
• double mutant exhibits increased (3172 pg/ml v. 662 pg/ml) total deposits relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• ratio of Abeta40:Abeta42 in double mutant is increased (3.8 : 1.5) relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• deposits are observed by 52 weeks of age (J:143551)
• double mutant exhibits increased (3172 pg/ml v. 662 pg/ml) total deposits relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• ratio of Abeta40:Abeta42 in double mutant is increased (3.8 : 1.5) relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• neuronal loss in hippocampus, subiculum and CA3 is significantly greater in double mutant relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• neuronal loss in hippocampus, subiculum and CA3 is significantly greater in double mutant relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• neuronal loss in hippocampus, subiculum and CA3 is significantly greater in double mutant relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• neuronal loss in hippocampus, subiculum and CA3 is significantly greater in double mutant relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• neuronal loss in subiculum is significantly greater in double mutant relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• neuronal loss in subiculum is significantly greater in double mutant relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• widespread cortical neuron damage (J:112919)
• widespread cortical neuron damage (J:112919)

behavior/neurological
• higher level of errors in day 2 of radial arm water maze in double mutant relative to single mutants Tg(APPSWE)2576Kha or homozygous Nostm1Lau (J:143551)
• higher level of errors in day 2 of radial arm water maze in double mutant relative to single mutants Tg(APPSWE)2576Kha or homozygous Nostm1Lau (J:143551)

homeostasis/metabolism
• plaque levels elevated in the brain relative to control mice carrying the transgene only (J:112919)
• plaque levels elevated in the brain relative to control mice carrying the transgene only (J:112919)
• deposits are observed by 52 weeks of age (J:143551)
• double mutant exhibits increased (3172 pg/ml v. 662 pg/ml) total deposits relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• ratio of Abeta40:Abeta42 in double mutant is increased (3.8 : 1.5) relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• deposits are observed by 52 weeks of age (J:143551)
• double mutant exhibits increased (3172 pg/ml v. 662 pg/ml) total deposits relative to control transgenic Tg(APPSWE)2576Kha (J:143551)
• ratio of Abeta40:Abeta42 in double mutant is increased (3.8 : 1.5) relative to control transgenic Tg(APPSWE)2576Kha (J:143551)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:112919




Genotype
MGI:4355224
cx4
Allelic
Composition
Apoetm2(APOE*3)Mae/Apoetm2(APOE*3)Mae
Tg(APPSWE)2576Kha/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm2(APOE*3)Mae mutation (1 available); any Apoe mutation (64 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• less plaque development than in Tg(APPSWE)2576Kha, Apoetm3(APOE*4Mae mice (J:98636)
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• less plaque development than in Tg(APPSWE)2576Kha, Apoetm3(APOE*4Mae mice (J:98636)

homeostasis/metabolism
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• less plaque development than in Tg(APPSWE)2576Kha, Apoetm3(APOE*4Mae mice (J:98636)
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• less plaque development than in Tg(APPSWE)2576Kha, Apoetm3(APOE*4Mae mice (J:98636)




Genotype
MGI:4355229
cx5
Allelic
Composition
Apoetm3(APOE*4)Mae/Apoetm3(APOE*4)Mae
Tg(APPSWE)2576Kha/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoetm3(APOE*4)Mae mutation (3 available); any Apoe mutation (64 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels with very few parenchymal plaques at 15 months (J:98636)
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels with very few parenchymal plaques at 15 months (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels (J:98636)

homeostasis/metabolism
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels with very few parenchymal plaques at 15 months (J:98636)
• increased levels of Amyloid beta 1-40 in cortical extracts at 3 months of age (J:98636)
• increased ratio of Amyloid beta 40:42 in cortical extracts at 3 months of age (J:98636)
• decreased ratio of Amyloid beta 40:42 in cerebrospinal fluid at 3 months of age (J:98636)
• deposition delayed until after 12 months of age (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels with very few parenchymal plaques at 15 months (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels (J:98636)
• Amyloid beta deposition starts around 12-15 months of age (J:98636)
• deposition is almost exclusively in cerebral blood vessels (J:98636)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:98636




Genotype
MGI:5306777
cx6
Allelic
Composition
Vps35Gt(RRK261)Byg/Vps35+
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
Vps35Gt(RRK261)Byg mutation (1 available); any Vps35 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• mice exhibit normal paired-pulse facilitation and inhibitory synaptic transmission (J:178937)
• mice exhibit normal paired-pulse facilitation and inhibitory synaptic transmission (J:178937)
• in the hippocampus and cerebral cortex (J:178937)
• greater accumulation than in Tg(APPSWE)2576Kha mice (J:178937)
• in the hippocampus and cerebral cortex (J:178937)
• greater accumulation than in Tg(APPSWE)2576Kha mice (J:178937)
• accelerated compared to in Tg(APPSWE)2576Kha mice (J:178937)
• accelerated compared to in Tg(APPSWE)2576Kha mice (J:178937)
• field excitatory postsynaptic potential slopes in the CA1 and dentate gyrus are reduced compared to in either single heterozygotes (J:178937)
• field excitatory postsynaptic potential slopes in the CA1 and dentate gyrus are reduced compared to in either single heterozygotes (J:178937)
• mice exhibit reduced AMPA and NMDA receptor-mediated miniature excitatory postsynaptic currents in CA1 pyramidal neurons compared with control mice (J:178937)
• mice exhibit reduced AMPA and NMDA receptor-mediated miniature excitatory postsynaptic currents in CA1 pyramidal neurons compared with control mice (J:178937)
• mice exhibit reduced AMPA and NMDA receptor-mediated miniature excitatory postsynaptic currents in CA1 pyramidal neurons compared with control mice (J:178937)
• mice exhibit reduced AMPA and NMDA receptor-mediated miniature excitatory postsynaptic currents in CA1 pyramidal neurons compared with control mice (J:178937)
• in the CA1 at 2 months (J:178937)
• worsened at 4 months in the CA1 (J:178937)
• however, long term potentiation in the dentate gyrus is normal (J:178937)
• in the CA1 at 2 months (J:178937)
• worsened at 4 months in the CA1 (J:178937)
• however, long term potentiation in the dentate gyrus is normal (J:178937)
• mice exhibit reduced AMPA and NMDA receptor-mediated miniature excitatory postsynaptic currents in CA1 pyramidal neurons compared with control mice (J:178937)
• mice exhibit reduced AMPA and NMDA receptor-mediated miniature excitatory postsynaptic currents in CA1 pyramidal neurons compared with control mice (J:178937)
• at 4 months in the CA1 (J:178937)
• at 4 months in the CA1 (J:178937)

behavior/neurological
• in a Morris water maze, mice exhibit increased latencies to finding the hidden platform and in pathway length compared with either single heterozygote (J:178937)
• deficits increase with age (J:178937)
• in a Morris water maze, mice exhibit increased latencies to finding the hidden platform and in pathway length compared with either single heterozygote (J:178937)
• deficits increase with age (J:178937)

homeostasis/metabolism
• in the hippocampus and cerebral cortex (J:178937)
• greater accumulation than in Tg(APPSWE)2576Kha mice (J:178937)
• in the hippocampus and cerebral cortex (J:178937)
• greater accumulation than in Tg(APPSWE)2576Kha mice (J:178937)




Genotype
MGI:5292247
cx7
Allelic
Composition
Psen1tm1Mpm/Psen1tm1Mpm
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Psen1tm1Mpm mutation (2 available); any Psen1 mutation (22 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice accumulate more plaques than in Psen1tm1.1Tcs/Psen1tm1.1Tcs Tg(APPSWE)2576Kha mice (J:175901)
• mice accumulate more plaques than in Psen1tm1.1Tcs/Psen1tm1.1Tcs Tg(APPSWE)2576Kha mice (J:175901)

homeostasis/metabolism
• mice accumulate more plaques than in Psen1tm1.1Tcs/Psen1tm1.1Tcs Tg(APPSWE)2576Kha mice (J:175901)
• mice accumulate more plaques than in Psen1tm1.1Tcs/Psen1tm1.1Tcs Tg(APPSWE)2576Kha mice (J:175901)




Genotype
MGI:2652383
cx8
Allelic
Composition
Psen1tm1Dgf/Psen1+
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * CD-1 * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Psen1tm1Dgf mutation (0 available); any Psen1 mutation (22 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• accelerated onset of amyloid plaque deposition and increased amyloidogenic processing of APP compared to single Tg(APPSWE)2576Kha mice (J:66147)
• accelerated onset of amyloid plaque deposition and increased amyloidogenic processing of APP compared to single Tg(APPSWE)2576Kha mice (J:66147)
• mutants exhibit enhanced reactive gliosis compared to single Tg(APPSWE)2576Kha mice (J:66147)
• mutants exhibit enhanced reactive gliosis compared to single Tg(APPSWE)2576Kha mice (J:66147)

homeostasis/metabolism
• accelerated onset of amyloid plaque deposition and increased amyloidogenic processing of APP compared to single Tg(APPSWE)2576Kha mice (J:66147)
• accelerated onset of amyloid plaque deposition and increased amyloidogenic processing of APP compared to single Tg(APPSWE)2576Kha mice (J:66147)




Genotype
MGI:2653196
cx9
Allelic
Composition
Cd40lgtm1Flv/Cd40lgtm1Flv
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd40lgtm1Flv mutation (1 available); any Cd40lg mutation (7 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• no detectable plaques at 12 months of age compared to minimal levels in mice carrying the transgene alone (J:80429)
• 41-51% reduction in beta-amyloid at 16 months as compared to transgene controls (J:80429)
• reduced numbers of large and medium sized plaques in the neocortex and hippocampus (J:80429)
• beta-CTF is reduced relative to alpha-CTF (J:80429)
• no detectable plaques at 12 months of age compared to minimal levels in mice carrying the transgene alone (J:80429)
• 41-51% reduction in beta-amyloid at 16 months as compared to transgene controls (J:80429)
• reduced numbers of large and medium sized plaques in the neocortex and hippocampus (J:80429)
• beta-CTF is reduced relative to alpha-CTF (J:80429)
• microgliosis and astrocytosis reduced (J:80429)
• microgliosis and astrocytosis reduced (J:80429)

homeostasis/metabolism
• no detectable plaques at 12 months of age compared to minimal levels in mice carrying the transgene alone (J:80429)
• 41-51% reduction in beta-amyloid at 16 months as compared to transgene controls (J:80429)
• reduced numbers of large and medium sized plaques in the neocortex and hippocampus (J:80429)
• beta-CTF is reduced relative to alpha-CTF (J:80429)
• no detectable plaques at 12 months of age compared to minimal levels in mice carrying the transgene alone (J:80429)
• 41-51% reduction in beta-amyloid at 16 months as compared to transgene controls (J:80429)
• reduced numbers of large and medium sized plaques in the neocortex and hippocampus (J:80429)
• beta-CTF is reduced relative to alpha-CTF (J:80429)

Mouse Models of Human Disease
OMIM ID Ref(s)
NOT Immunodeficiency with Hyper-IgM, Type 1; HIGM1 308230 J:80429




Genotype
MGI:4831171
cx10
Allelic
Composition
Ccr2tm1Ifc/Ccr2+
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccr2tm1Ifc mutation (1 available); any Ccr2 mutation (6 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by 130 days, 60% of mice are dead compared with 30% of mice expressing Tg(APPSWE)2576Kha, 1% of wild-type mice, and 3% of Ccr2tm1Ifc homozygotes (J:121703)
• by 130 days, 60% of mice are dead compared with 30% of mice expressing Tg(APPSWE)2576Kha, 1% of wild-type mice, and 3% of Ccr2tm1Ifc homozygotes (J:121703)




Genotype
MGI:4831169
cx11
Allelic
Composition
Ccr2tm1Ifc/Ccr2tm1Ifc
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ccr2tm1Ifc mutation (1 available); any Ccr2 mutation (6 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• by 130 days, 85% of mice are dead compared with 30% of mice expressing Tg(APPSWE)2576Kha, 1% of wild-type mice, and 3% of Ccr2tm1Ifc homozygotes (J:121703)
• by 130 days, 85% of mice are dead compared with 30% of mice expressing Tg(APPSWE)2576Kha, 1% of wild-type mice, and 3% of Ccr2tm1Ifc homozygotes (J:121703)

nervous system
• microglia accumulation is impaired compared to in mice expressing Tg(APPSWE)2576Kha (J:121703)
• however, microglial proliferation and responses to beta-amyloid are normal (J:121703)
• microglia accumulation is impaired compared to in mice expressing Tg(APPSWE)2576Kha (J:121703)
• however, microglial proliferation and responses to beta-amyloid are normal (J:121703)
• at P65 without classic plaques (J:121703)
• at P65 without classic plaques (J:121703)

immune system
• microglia accumulation is impaired compared to in mice expressing Tg(APPSWE)2576Kha (J:121703)
• however, microglial proliferation and responses to beta-amyloid are normal (J:121703)
• microglia accumulation is impaired compared to in mice expressing Tg(APPSWE)2576Kha (J:121703)
• however, microglial proliferation and responses to beta-amyloid are normal (J:121703)

cardiovascular system

hematopoietic system
• microglia accumulation is impaired compared to in mice expressing Tg(APPSWE)2576Kha (J:121703)
• however, microglial proliferation and responses to beta-amyloid are normal (J:121703)
• microglia accumulation is impaired compared to in mice expressing Tg(APPSWE)2576Kha (J:121703)
• however, microglial proliferation and responses to beta-amyloid are normal (J:121703)

homeostasis/metabolism
• at P65, accumulation of beta-amyloid 1-42 and 1-40 in the brain are 2.4-fold and 1.4-fold respectively compared to in mice expressing Tg(APPSWE)2576Kha (J:121703)
• at P65, accumulation of beta-amyloid 1-42 and 1-40 in the brain are 2.4-fold and 1.4-fold respectively compared to in mice expressing Tg(APPSWE)2576Kha (J:121703)
• at P65 without classic plaques (J:121703)
• at P65 without classic plaques (J:121703)




Genotype
MGI:3810279
cx12
Allelic
Composition
Dab1tm1Bwh/Dab1tm1Bwh
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dab1tm1Bwh mutation (0 available); any Dab1 mutation (10 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• the loss of divisions between some folia is apparent (J:132599)
• the loss of divisions between some folia is apparent (J:132599)
• the vermis to whole brain ratio is smaller than in Dab1tm1Bwh homozygotes (J:132599)
• the vermis to whole brain ratio is smaller than in Dab1tm1Bwh homozygotes (J:132599)




Genotype
MGI:3663101
cx13
Allelic
Composition
Appd1FVB/NCr/Appd1FVB/NCr
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * FVB/NCr * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Appd1FVB/NCr mutation (0 available); any Appd1 mutation (0 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:3663102
cx14
Allelic
Composition
Appd2FVB/NCr/Appd2FVB/NCr
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * FVB/NCr * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Appd2FVB/NCr mutation (0 available); any Appd2 mutation (0 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:3624416
cx15
Allelic
Composition
Psen1tm1Zhe/Psen1tm1Zhe
Tg(APPSWE)2576Kha/?
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Psen1tm1Zhe mutation (0 available); any Psen1 mutation (22 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• dramatically higher plaque density in brain compared to control Tg(APPSWE)2576Kahs transgenic mice (J:107251)
• numerous plaques could be detected in both the cortex and hippocampus at 10 month (J:107251)
• dramatically higher plaque density in brain compared to control Tg(APPSWE)2576Kahs transgenic mice (J:107251)
• numerous plaques could be detected in both the cortex and hippocampus at 10 month (J:107251)

homeostasis/metabolism
• dramatically higher plaque density in brain compared to control Tg(APPSWE)2576Kahs transgenic mice (J:107251)
• numerous plaques could be detected in both the cortex and hippocampus at 10 month (J:107251)
• dramatically higher plaque density in brain compared to control Tg(APPSWE)2576Kahs transgenic mice (J:107251)
• numerous plaques could be detected in both the cortex and hippocampus at 10 month (J:107251)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:107251




Genotype
MGI:3029279
cx16
Allelic
Composition
Slc30a3tm1Rpa/Slc30a3tm1Rpa
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc30a3tm1Rpa mutation (1 available); any Slc30a3 mutation (1 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• plaque formation and insoluble amyloid beta levels are reduced relative to hemizygous Tg(APPSWE)2576HKahs mice that carried two wild copies of Slc30a3 (J:76863)
• no sexual difference in synaptic zinc levels, plaque formation, or insoluble amyloid beta levels (J:76863)
• plaques are smaller in size than in single Tg(APPSWE)2576Kha hemizygotes (J:76863)
• mutants exhibit an increased ratio of souluble/insoluble amyloid beta at 18 months of age compared to single Tg(APPSWE)2576Kha hemizygotes (J:76863)
• plaque formation and insoluble amyloid beta levels are reduced relative to hemizygous Tg(APPSWE)2576HKahs mice that carried two wild copies of Slc30a3 (J:76863)
• no sexual difference in synaptic zinc levels, plaque formation, or insoluble amyloid beta levels (J:76863)
• plaques are smaller in size than in single Tg(APPSWE)2576Kha hemizygotes (J:76863)
• mutants exhibit an increased ratio of souluble/insoluble amyloid beta at 18 months of age compared to single Tg(APPSWE)2576Kha hemizygotes (J:76863)

homeostasis/metabolism
• males and females exhibit a decrease in levels of synaptic and total zinc compared to single Tg(APPSWE)2576Kha hemizygotes (J:76863)
• males and females exhibit a decrease in levels of synaptic and total zinc compared to single Tg(APPSWE)2576Kha hemizygotes (J:76863)
• plaque formation and insoluble amyloid beta levels are reduced relative to hemizygous Tg(APPSWE)2576HKahs mice that carried two wild copies of Slc30a3 (J:76863)
• no sexual difference in synaptic zinc levels, plaque formation, or insoluble amyloid beta levels (J:76863)
• plaques are smaller in size than in single Tg(APPSWE)2576Kha hemizygotes (J:76863)
• mutants exhibit an increased ratio of souluble/insoluble amyloid beta at 18 months of age compared to single Tg(APPSWE)2576Kha hemizygotes (J:76863)
• plaque formation and insoluble amyloid beta levels are reduced relative to hemizygous Tg(APPSWE)2576HKahs mice that carried two wild copies of Slc30a3 (J:76863)
• no sexual difference in synaptic zinc levels, plaque formation, or insoluble amyloid beta levels (J:76863)
• plaques are smaller in size than in single Tg(APPSWE)2576Kha hemizygotes (J:76863)
• mutants exhibit an increased ratio of souluble/insoluble amyloid beta at 18 months of age compared to single Tg(APPSWE)2576Kha hemizygotes (J:76863)




Genotype
MGI:4367205
cx17
Allelic
Composition
Ldlrtm1Her/Ldlrtm1Her
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ldlrtm1Her mutation (18 available); any Ldlr mutation (46 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• make more entries into the open arms of an elevated plus maze on day 2 of testing (J:114480)
• make more entries into the open arms of an elevated plus maze on day 2 of testing (J:114480)
• fail to show intersession habituation over 3 days of testing in an open field, unlike transgenic mice wild-type for Ldlr (J:114480)
• fail to show intersession habituation over 3 days of testing in an open field, unlike transgenic mice wild-type for Ldlr (J:114480)
• learning impairment in a Morris water maze at 10 months of age (J:114480)
• impairment not affected by Ldlr genotype (J:114480)
• learning impairment in a Morris water maze at 10 months of age (J:114480)
• impairment not affected by Ldlr genotype (J:114480)
• at 13 months of age mice trained at 10 months of age are slower to reacquire the location of the hidden platform in a morris water maze compared to transgenic mice wild-type for Ldlr (J:114480)
• in a probe trial mice fail to occupy the target quadrant longer than chance indicating memory retention deficits (J:114480)
• at 13 months of age mice trained at 10 months of age are slower to reacquire the location of the hidden platform in a morris water maze compared to transgenic mice wild-type for Ldlr (J:114480)
• in a probe trial mice fail to occupy the target quadrant longer than chance indicating memory retention deficits (J:114480)
• relative to non-transgenic controls (J:114480)
• relative to non-transgenic controls (J:114480)

homeostasis/metabolism
• hypercholesterolemia with the increase in the non-HDL fraction (J:114480)
• hypercholesterolemia with the increase in the non-HDL fraction (J:114480)
• increase is mainly in the LDL fraction (J:114480)
• increase is mainly in the LDL fraction (J:114480)
• age dependent cerebral amyloidosis (J:114480)
• plaques first appear in the hippocampus and cortex at around 11 months (J:114480)
• progressive accumulation in the brain after 11 months (J:114480)
• age dependent cerebral amyloidosis (J:114480)
• plaques first appear in the hippocampus and cortex at around 11 months (J:114480)
• progressive accumulation in the brain after 11 months (J:114480)
• cerebral amyloid beta deposition is increased compared to transgenic mice wild-type for Ldlr (J:114480)
• cerebral amyloid beta deposition is increased compared to transgenic mice wild-type for Ldlr (J:114480)

nervous system
• cerebral amyloid beta deposition is increased compared to transgenic mice wild-type for Ldlr (J:114480)
• cerebral amyloid beta deposition is increased compared to transgenic mice wild-type for Ldlr (J:114480)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:114480




Genotype
MGI:4880015
cx18
Allelic
Composition
Pld2tm1.1Gdp/Pld2+
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pld2tm1.1Gdp mutation (0 available); any Pld2 mutation (3 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice exhibit normal spatial working memory unlike Tg(APPSWE)2576Kha mice (J:166741)
• mice exhibit normal spatial working memory unlike Tg(APPSWE)2576Kha mice (J:166741)
• compared to Tg(APPSWE)2576Kha mice (J:166741)
• compared to Tg(APPSWE)2576Kha mice (J:166741)




Genotype
MGI:4880014
cx19
Allelic
Composition
Pld2tm1.1Gdp/Pld2tm1.1Gdp
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pld2tm1.1Gdp mutation (0 available); any Pld2 mutation (3 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• mice exhibit normal spatial working memory unlike Tg(APPSWE)2576Kha mice (J:166741)
• mice exhibit normal spatial working memory unlike Tg(APPSWE)2576Kha mice (J:166741)
• compared to Tg(APPSWE)2576Kha mice (J:166741)
• compared to Tg(APPSWE)2576Kha mice (J:166741)

homeostasis/metabolism
• mice exhibit altered levels of specific phosphatidic acids compared to in wild-type mice (J:166741)
• mice exhibit altered levels of specific phosphatidic acids compared to in wild-type mice (J:166741)

nervous system
• mice exhibit synaptic protection compared to in Tg(APPSWE)2576Kha mice (J:166741)
• mice exhibit synaptic protection compared to in Tg(APPSWE)2576Kha mice (J:166741)




Genotype
MGI:4836978
cx20
Allelic
Composition
Hspa4tm1.1Miv/Hspa4tm1.1Miv
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: BALB/cJ * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hspa4tm1.1Miv mutation (0 available); any Hspa4 mutation (48 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• many mice die before 7 months of age (J:164904)
• many mice die before 7 months of age (J:164904)

nervous system
• at 6 months, mice develop neurofibril tangles unlike Tg(APPSWE)2576Kha mice (J:164904)
• at 7 months, mice develop senility plaques unlike Tg(APPSWE)2576Kha mice (J:164904)
• at 6 months, mice develop neurofibril tangles unlike Tg(APPSWE)2576Kha mice (J:164904)
• at 7 months, mice develop senility plaques unlike Tg(APPSWE)2576Kha mice (J:164904)
• neuron degeneration is more severe than in Tg(APPSWE)2576Kha mice (J:164904)
• neuron degeneration is more severe than in Tg(APPSWE)2576Kha mice (J:164904)




Genotype
MGI:3710765
cx21
Allelic
Composition
Tg(APPSWE)2576Kha/0
Tg(Prnp-ITM2B/APP695*42)A12Emcg/0
Genetic
Background
involves: C3H * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
Tg(Prnp-ITM2B/APP695*42)A12Emcg mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• augmentation of Abeta deposits throughout cortex, hippocampus, and cerebellum is observed in double transgenic mice at 14.5 month-old mice, relative to single transgenics (J:101023)
• augmentation of Abeta deposits throughout cortex, hippocampus, and cerebellum is observed in double transgenic mice at 14.5 month-old mice, relative to single transgenics (J:101023)
• mice show enhanced senile plaque pathology in the forebrain at 14.5 months (J:101023)
• mice show enhanced senile plaque pathology in the forebrain at 14.5 months (J:101023)
• mice show elevated insoluble Abeta levels in the hindbrain at 14.5 months (J:101023)
• mice show elevated insoluble Abeta levels in the hindbrain at 14.5 months (J:101023)

homeostasis/metabolism
• formic acid extractable Abeta40 and Abeta42 levels are dramatically elevated at 14.5 months in hindbrain compared Tg(APPSWE)2576Kahs single transgenic mice; levels of Abeta42 are slightly higher than those observed in forebrains of Tg(Prnp-ITM2B/APP695*42)A12Emcg mice at 14.5 months, while Abeta40 levels are significantly higher than in either single transgenic mouse (J:101023)
• formic acid extractable Abeta40 and Abeta42 levels are dramatically elevated at 14.5 months in hindbrain compared Tg(APPSWE)2576Kahs single transgenic mice; levels of Abeta42 are slightly higher than those observed in forebrains of Tg(Prnp-ITM2B/APP695*42)A12Emcg mice at 14.5 months, while Abeta40 levels are significantly higher than in either single transgenic mouse (J:101023)
• augmentation of Abeta deposits throughout cortex, hippocampus, and cerebellum is observed in double transgenic mice at 14.5 month-old mice, relative to single transgenics (J:101023)
• augmentation of Abeta deposits throughout cortex, hippocampus, and cerebellum is observed in double transgenic mice at 14.5 month-old mice, relative to single transgenics (J:101023)




Genotype
MGI:5292246
cx22
Allelic
Composition
Psen1tm1.1Tcs/Psen1tm1.1Tcs
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: C57BL/6 * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Psen1tm1.1Tcs mutation (0 available); any Psen1 mutation (22 available)
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• at 3 to 4 months in a Y-maze test (J:175901)
• at 3 to 4 months in a Y-maze test (J:175901)

nervous system
• beginning at 6 months, earlier than in Tg(APPSWE)2576Kha mice at 12 months (J:175901)
• fewer plaques than in Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSWE)2576Kha mice (J:175901)
• beginning at 6 months, earlier than in Tg(APPSWE)2576Kha mice at 12 months (J:175901)
• fewer plaques than in Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSWE)2576Kha mice (J:175901)
• at 9 months (J:175901)
• at 9 months (J:175901)

homeostasis/metabolism
• beginning at 6 months, earlier than in Tg(APPSWE)2576Kha mice at 12 months (J:175901)
• fewer plaques than in Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSWE)2576Kha mice (J:175901)
• beginning at 6 months, earlier than in Tg(APPSWE)2576Kha mice at 12 months (J:175901)
• fewer plaques than in Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSWE)2576Kha mice (J:175901)




Genotype
MGI:3717259
cx23
Allelic
Composition
Tg(APPSWE)2576Kha/0
Tg(PDGFB-PSEN1M146L)2Jhd/0
Genetic
Background
involves: C57BL/6 * DBA/2 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
Tg(PDGFB-PSEN1M146L)2Jhd mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at <3 months of age, mice show amyloid beta deposits in frontal cortex; with age, deposits spread throughout cortex, and to the hippocampus, thalamus and dentate gyrus (J:68670)
• by 1 year of age, deposits are widely observed, with no apparent increase in total amount of amyloid deposited after this age (J:68670)
• some fibrillar amyloid beta deposits are detected in the frontal cortex of youngest mice, with absence of deposits in more caudal regions; number of fibrillar deposits increases up to 1 year of age, with area covered by fibrillar deposits increasing up to 2 years of age (J:68670)
• at 1 year, area covered by fibrillar deposits is ~50% of total amyloid beta, but comprises majority of total covered area by 2.5 years of age (J:68670)
• at <3 months of age, mice show amyloid beta deposits in frontal cortex; with age, deposits spread throughout cortex, and to the hippocampus, thalamus and dentate gyrus (J:68670)
• by 1 year of age, deposits are widely observed, with no apparent increase in total amount of amyloid deposited after this age (J:68670)
• some fibrillar amyloid beta deposits are detected in the frontal cortex of youngest mice, with absence of deposits in more caudal regions; number of fibrillar deposits increases up to 1 year of age, with area covered by fibrillar deposits increasing up to 2 years of age (J:68670)
• at 1 year, area covered by fibrillar deposits is ~50% of total amyloid beta, but comprises majority of total covered area by 2.5 years of age (J:68670)
• ins some areas of cortex in older animals,astrocytes appear dystrophic and are no longer closely associated with plaques, although nearby plaques are associated with activated glial cells (J:68670)
• ins some areas of cortex in older animals,astrocytes appear dystrophic and are no longer closely associated with plaques, although nearby plaques are associated with activated glial cells (J:68670)
• activated microglia accumulate around amyloid beta deposits from ~ 3 months; number of glia increases with age and amyloid accumulation (J:68670)
• activated microglia accumulate around amyloid beta deposits from ~ 3 months; number of glia increases with age and amyloid accumulation (J:68670)
• activated astrocytes accumulate around amyloid deposits in frontal cortex of 3 month old mice (J:68670)
• activated astrocytes accumulate around amyloid deposits in frontal cortex of 3 month old mice (J:68670)

homeostasis/metabolism
• at <3 months of age, mice show amyloid beta deposits in frontal cortex; with age, deposits spread throughout cortex, and to the hippocampus, thalamus and dentate gyrus (J:68670)
• by 1 year of age, deposits are widely observed, with no apparent increase in total amount of amyloid deposited after this age (J:68670)
• some fibrillar amyloid beta deposits are detected in the frontal cortex of youngest mice, with absence of deposits in more caudal regions; number of fibrillar deposits increases up to 1 year of age, with area covered by fibrillar deposits increasing up to 2 years of age (J:68670)
• at 1 year, area covered by fibrillar deposits is ~50% of total amyloid beta, but comprises majority of total covered area by 2.5 years of age (J:68670)
• at <3 months of age, mice show amyloid beta deposits in frontal cortex; with age, deposits spread throughout cortex, and to the hippocampus, thalamus and dentate gyrus (J:68670)
• by 1 year of age, deposits are widely observed, with no apparent increase in total amount of amyloid deposited after this age (J:68670)
• some fibrillar amyloid beta deposits are detected in the frontal cortex of youngest mice, with absence of deposits in more caudal regions; number of fibrillar deposits increases up to 1 year of age, with area covered by fibrillar deposits increasing up to 2 years of age (J:68670)
• at 1 year, area covered by fibrillar deposits is ~50% of total amyloid beta, but comprises majority of total covered area by 2.5 years of age (J:68670)




Genotype
MGI:3720702
cx24
Allelic
Composition
Tg(APPSWE)2576Kha/0
Tg(Prnp-MAPT*P301L)JNPL3Hlmc/0
Genetic
Background
involves: C57BL/6 * DBA/2 * SJL * SW
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
Tg(Prnp-MAPT*P301L)JNPL3Hlmc mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• progressive hindlimb weakness is observed (J:100965)
• progressive hindlimb weakness is observed (J:100965)
• reduced (J:100965)
• reduced (J:100965)

nervous system
• mice have amyloid plaques similar in number and distribution to Tg(APPSWE)2576Kha mice; plaques are detected as early as 6 months, but do become numerous only in older mice (8.5 to 15 months) in the olfactory cortex, cingulated gyrus, amygdala, entorhinal cortex, and hippocampus (J:100965)
• deposits contain both Abeta1-40 and Abeta1-42 peptides (J:100965)
• mice have amyloid plaques similar in number and distribution to Tg(APPSWE)2576Kha mice; plaques are detected as early as 6 months, but do become numerous only in older mice (8.5 to 15 months) in the olfactory cortex, cingulated gyrus, amygdala, entorhinal cortex, and hippocampus (J:100965)
• deposits contain both Abeta1-40 and Abeta1-42 peptides (J:100965)
• by 3 months of age, neurofibrillary tangles (NFTs) composed of straight fibers sometimes forming complex structures are detected in the spinal cords and pons of transgenic animals, and become more numerous with age (J:100965)
• older females 9-11 months of age display marked increases in NFTs in limbic areas, such as the olfactory cortex, entorhinal cortex, and amygdala; density of NFTs in females is >7-fold higher than in Tg(Prnp-MAPT*P301L)JNPL3 littermates (J:100965)
• norm male animals do not develop enhanced NFT pathology in limbic regions (J:100965)
• NFTs are also found in subiculum, hippocampus and sometimes in the isocortex, whereas NFTs are never or rarely observed in these brain regions of Tg(Prnp-MAPT*P301L)JNPL3 animals (J:100965)
• number and distribution of pretangles is increased in 9-11 month-old mice in limbic areas and cerebral cortex (J:100965)
• by 3 months of age, neurofibrillary tangles (NFTs) composed of straight fibers sometimes forming complex structures are detected in the spinal cords and pons of transgenic animals, and become more numerous with age (J:100965)
• older females 9-11 months of age display marked increases in NFTs in limbic areas, such as the olfactory cortex, entorhinal cortex, and amygdala; density of NFTs in females is >7-fold higher than in Tg(Prnp-MAPT*P301L)JNPL3 littermates (J:100965)
• norm male animals do not develop enhanced NFT pathology in limbic regions (J:100965)
• NFTs are also found in subiculum, hippocampus and sometimes in the isocortex, whereas NFTs are never or rarely observed in these brain regions of Tg(Prnp-MAPT*P301L)JNPL3 animals (J:100965)
• number and distribution of pretangles is increased in 9-11 month-old mice in limbic areas and cerebral cortex (J:100965)
• levels of soluble endogenous and transgenic Tau protein are similar to Tg(Prnp-MAPT*P301L)JNPL3Hlmc transgenic mice; 64-kd insoluble tau species in increased in cortex/limbic regions of females 9-11 months compared to Tg(Prnp-MAPT*P301L)JNPL3Hlmc mice (J:100965)
• levels of soluble endogenous and transgenic Tau protein are similar to Tg(Prnp-MAPT*P301L)JNPL3Hlmc transgenic mice; 64-kd insoluble tau species in increased in cortex/limbic regions of females 9-11 months compared to Tg(Prnp-MAPT*P301L)JNPL3Hlmc mice (J:100965)
• as severe as astrocytosis in ventral diencepalon, hindbrain, and spinal cord (J:100965)
• as severe as astrocytosis in ventral diencepalon, hindbrain, and spinal cord (J:100965)
• increase observed in limbic areas with the most NFTs (J:100965)
• increase observed in limbic areas with the most NFTs (J:100965)
• Tau filaments occupy large proportion of cell volume, displacing nucleus and cytoplasmic organelles and compressing the Golgi apparatus (J:100965)
• dystrophic neurites reactive for APP epitopes are associated with amyloid plaques (J:100965)
• Tau filaments occupy large proportion of cell volume, displacing nucleus and cytoplasmic organelles and compressing the Golgi apparatus (J:100965)
• dystrophic neurites reactive for APP epitopes are associated with amyloid plaques (J:100965)
• neurofibrillary degeneration resulting from accumulation of NFTs is observed as early as 6 months (J:100965)
• granulovacuolar degeneration is seen in neurons of amygdala, entorhinal cortex, and subiculum of females, characterized by optically clear vacuoles with dense cores (J:100965)
• neurofibrillary degeneration resulting from accumulation of NFTs is observed as early as 6 months (J:100965)
• granulovacuolar degeneration is seen in neurons of amygdala, entorhinal cortex, and subiculum of females, characterized by optically clear vacuoles with dense cores (J:100965)

vision/eye
• increased eye irritation (J:100965)
• increased eye irritation (J:100965)

homeostasis/metabolism
• mice have amyloid plaques similar in number and distribution to Tg(APPSWE)2576Kha mice; plaques are detected as early as 6 months, but do become numerous only in older mice (8.5 to 15 months) in the olfactory cortex, cingulated gyrus, amygdala, entorhinal cortex, and hippocampus (J:100965)
• deposits contain both Abeta1-40 and Abeta1-42 peptides (J:100965)
• mice have amyloid plaques similar in number and distribution to Tg(APPSWE)2576Kha mice; plaques are detected as early as 6 months, but do become numerous only in older mice (8.5 to 15 months) in the olfactory cortex, cingulated gyrus, amygdala, entorhinal cortex, and hippocampus (J:100965)
• deposits contain both Abeta1-40 and Abeta1-42 peptides (J:100965)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:100965




Genotype
MGI:3711709
cx25
Allelic
Composition
Tg(APPSWE)2576Kha/?
Tg(PDGFB-PSEN1M146L)2Jhd/?
Genetic
Background
involves: C57BL/6 * DBA/2 * SJL * SW
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
Tg(PDGFB-PSEN1M146L)2Jhd mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• treatment with antibody to CD40L results in more diffuse beta-amyloid plaques (J:80429)
• equal levels of alpha- and beta-CTF (J:80429)
• antibody to CD40L produces increased levels of circulating beta amyloid (J:80429)
• treatment with antibody to CD40L results in more diffuse beta-amyloid plaques (J:80429)
• equal levels of alpha- and beta-CTF (J:80429)
• antibody to CD40L produces increased levels of circulating beta amyloid (J:80429)
• microgliosis and astrocytosis reduced in the hippocampus, and entorhinal cortex (J:80429)
• astrocytosis also reduced in the cingulated cortex (J:80429)
• microgliosis and astrocytosis reduced in the hippocampus, and entorhinal cortex (J:80429)
• astrocytosis also reduced in the cingulated cortex (J:80429)

homeostasis/metabolism
• treatment with antibody to CD40L results in more diffuse beta-amyloid plaques (J:80429)
• equal levels of alpha- and beta-CTF (J:80429)
• antibody to CD40L produces increased levels of circulating beta amyloid (J:80429)
• treatment with antibody to CD40L results in more diffuse beta-amyloid plaques (J:80429)
• equal levels of alpha- and beta-CTF (J:80429)
• antibody to CD40L produces increased levels of circulating beta amyloid (J:80429)




Genotype
MGI:5140748
cx26
Allelic
Composition
Tg(APPSWE)2576Kha/0
Tg(PDGFB-PSEN1M146L)2Jhd/0
Genetic
Background
involves: C57BL/6 * DBA/2 * SJL * SW
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
Tg(PDGFB-PSEN1M146L)2Jhd mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• kidney glomeruli are dilated probably due to obstruction from the amyloid in the lumen or walls of medullary tubules especially in the papilla (J:174270)
• kidney glomeruli are dilated probably due to obstruction from the amyloid in the lumen or walls of medullary tubules especially in the papilla (J:174270)

homeostasis/metabolism
• some mutants older than 18 months exhibit amyloid deposits in the spleen and kidneys, and occasionally in the liver, ovary and/or heart (J:174270)
• amyloid is deposited concentrically in the perifollicular sheath, partly or completely encircling the follicles in the spleen (J:174270)
• in the liver, amyloid deposit is in the walls of sinusoids or central veins (J:174270)
• in the kidney, amyloid deposits are seen in the glomeruli (J:174270)
• amyloid deposits in the heart are not composed of amyloid-beta peptide, but rather amyloid A (J:174270)
• some mutants older than 18 months exhibit amyloid deposits in the spleen and kidneys, and occasionally in the liver, ovary and/or heart (J:174270)
• amyloid is deposited concentrically in the perifollicular sheath, partly or completely encircling the follicles in the spleen (J:174270)
• in the liver, amyloid deposit is in the walls of sinusoids or central veins (J:174270)
• in the kidney, amyloid deposits are seen in the glomeruli (J:174270)
• amyloid deposits in the heart are not composed of amyloid-beta peptide, but rather amyloid A (J:174270)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:174270




Genotype
MGI:5699096
cx27
Allelic
Composition
Tg(APPSWE)2576Kha/?
Tg(EIF1AX-Aldh2*E487K)101Oht/?
Genetic
Background
involves: C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
Tg(EIF1AX-Aldh2*E487K)101Oht mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants begin dying by 120 days of age and death rate accelerates after 240 days compared to either single mutant (J:219346)
• mutants begin dying by 120 days of age and death rate accelerates after 240 days compared to either single mutant (J:219346)

growth/size/body
• mutants weigh less than wild-type mice and single Tg(EIF1AX-Aldh2*E487K)101Oht mice, but exhibit no weight differences from single Tg(APPSWE)2576Kha mice (J:219346)
• mutants weigh less than wild-type mice and single Tg(EIF1AX-Aldh2*E487K)101Oht mice, but exhibit no weight differences from single Tg(APPSWE)2576Kha mice (J:219346)

behavior/neurological
• in the object recognition test, exploratory preference for the novel object is lower at 3 months of age compared to wild-type mice or either single mutant, and is lower at 6 months of age compared to wild-type mice or single Tg(EIF1AX-Aldh2*E487K)101Oht mice (J:219346)
• in the object recognition test, exploratory preference for the novel object is lower at 3 months of age compared to wild-type mice or either single mutant, and is lower at 6 months of age compared to wild-type mice or single Tg(EIF1AX-Aldh2*E487K)101Oht mice (J:219346)
• at 3 and 6 months of age, the alternation rate of Y-maze is lower than in wild-type mice or either single mutant (J:219346)
• at 3 and 6 months of age, the alternation rate of Y-maze is lower than in wild-type mice or either single mutant (J:219346)

homeostasis/metabolism
• amyloid beta plaques are detected in the brain at 6 months of age, a time when plaques are not seen in single Tg(APPSWE)2576Kha mice (J:219346)
• at 12-15 months of age, more amyloid beta40 and amyloid beta42 plaques are seen than in single Tg(APPSWE)2576Kha mice (J:219346)
• amyloid beta plaques are detected in the brain at 6 months of age, a time when plaques are not seen in single Tg(APPSWE)2576Kha mice (J:219346)
• at 12-15 months of age, more amyloid beta40 and amyloid beta42 plaques are seen than in single Tg(APPSWE)2576Kha mice (J:219346)

nervous system
• amyloid beta plaques are detected in the brain at 6 months of age, a time when plaques are not seen in single Tg(APPSWE)2576Kha mice (J:219346)
• at 12-15 months of age, more amyloid beta40 and amyloid beta42 plaques are seen than in single Tg(APPSWE)2576Kha mice (J:219346)
• amyloid beta plaques are detected in the brain at 6 months of age, a time when plaques are not seen in single Tg(APPSWE)2576Kha mice (J:219346)
• at 12-15 months of age, more amyloid beta40 and amyloid beta42 plaques are seen than in single Tg(APPSWE)2576Kha mice (J:219346)
• deposition of phosphorylated tau proteins in the brains is increased at 9 months of age compared to single Tg(APPSWE)2576Kha mice (J:219346)
• deposition of phosphorylated tau proteins in the brains is increased at 9 months of age compared to single Tg(APPSWE)2576Kha mice (J:219346)
• mutants show a greater number of astrocyte clusters in the CA1 region of the hippocampus and cerebral cortex at 6, 9, and 12 months of age than single Tg(APPSWE)2576Kha mice (J:219346)
• mutants show a greater number of astrocyte clusters in the CA1 region of the hippocampus and cerebral cortex at 6, 9, and 12 months of age than single Tg(APPSWE)2576Kha mice (J:219346)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:219346




Genotype
MGI:5463430
cx28
Allelic
Composition
Tg(APPSWE)2576Kha/0
Tg(PSEN1)5Dbo/0
Genetic
Background
involves: C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
Tg(PSEN1)5Dbo mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• dense amyloid beta plaques in the cortex and hippocampus, but not in the adrenal medulla (J:191088)
• dense amyloid beta plaques in the cortex and hippocampus, but not in the adrenal medulla (J:191088)
• amperometric recordings from chromaffin cells stimulated with a 10 second 70 mM potassium pulse indicate that the quantity of catecholamines released during the initiation of the fusion pore is 50% smaller in mutants than in controls (J:191088)
• chromaffin cells exhibit smaller quantal size and faster kinetics of single exocytotic events (45% lower spike half-width, 60% smaller quantal size, 50% lower decay time) and spike feet show 60% smaller quantal size (J:191088)
• mutants, however, exhibit normal innervation by splanchnic cholinergic nerve terminals of chromaffin cells (J:191088)
• amperometric recordings from chromaffin cells stimulated with a 10 second 70 mM potassium pulse indicate that the quantity of catecholamines released during the initiation of the fusion pore is 50% smaller in mutants than in controls (J:191088)
• chromaffin cells exhibit smaller quantal size and faster kinetics of single exocytotic events (45% lower spike half-width, 60% smaller quantal size, 50% lower decay time) and spike feet show 60% smaller quantal size (J:191088)
• mutants, however, exhibit normal innervation by splanchnic cholinergic nerve terminals of chromaffin cells (J:191088)

homeostasis/metabolism
• chromaffin cells release 50% less catecholamine (mean quantal content released per vesicle is halved) in response to a 10 second 70 mM potassium pulse (J:191088)
• chromaffin cells release 50% less catecholamine (mean quantal content released per vesicle is halved) in response to a 10 second 70 mM potassium pulse (J:191088)
• dense amyloid beta plaques in the cortex and hippocampus, but not in the adrenal medulla (J:191088)
• dense amyloid beta plaques in the cortex and hippocampus, but not in the adrenal medulla (J:191088)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:191088




Genotype
MGI:4366449
tg29
Allelic
Composition
Tg(APPSWE)2576Kha/Tg(APPSWE)2576Kha
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants die prematurely; time not specified (J:76863)
• mutants die prematurely; time not specified (J:76863)




Genotype
MGI:3722308
tg30
Allelic
Composition
Tg(APPSWE)2576Kha/0
Genetic
Background
FVB.Cg-Tg(APPSWE)2576Kha
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• Background Sensitivity: ~44% of mice die before 150 days of age (J:43446)
• Background Sensitivity: ~44% of mice die before 150 days of age (J:43446)

behavior/neurological
• Background Sensitivity: 25% of mice display neophobia compared to none on mixed genetic background (J:43446)
• Background Sensitivity: 25% of mice display neophobia compared to none on mixed genetic background (J:43446)




Genotype
MGI:3029285
tg31
Allelic
Composition
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• 12 month old mice exhibit normal motor coordination on the rotarod (J:180385)
• 12 month old mice exhibit normal motor coordination on the rotarod (J:180385)
• spend more time in the open arms of an elevated plus maze (J:114480)
• spend more time in the open arms of an elevated plus maze (J:114480)
• mutants exhibit impaired long-trace interval eyeblink conditioning at 6 months of age (J:180385)
• however, mutants do not exhibit impaired delay eyeblink conditioning even at 12 months of age, although it is slightly but insignificantly decreased (J:180385)
• mutants exhibit impaired long-trace interval eyeblink conditioning at 6 months of age (J:180385)
• however, mutants do not exhibit impaired delay eyeblink conditioning even at 12 months of age, although it is slightly but insignificantly decreased (J:180385)
• impaired spatial learning in a morris water maze (J:114480)
• impaired spatial learning in a morris water maze (J:114480)
• in a probe trial mice fail to occupy the target quadrant longer than chance indicating memory retention deficits (J:114480)
• in a probe trial mice fail to occupy the target quadrant longer than chance indicating memory retention deficits (J:114480)

homeostasis/metabolism
• females exhibit an increase in levels of synaptic zinc with aging (J:76863)
• females exhibit an increase in levels of synaptic zinc with aging (J:76863)
• increase in insoluble amyloid beta and plaques with aging; greater increase in plaques in females than males (J:76863)
• increase in insoluble amyloid beta and plaques with aging; greater increase in plaques in females than males (J:76863)

nervous system
• increase in insoluble amyloid beta and plaques with aging; greater increase in plaques in females than males (J:76863)
• increase in insoluble amyloid beta and plaques with aging; greater increase in plaques in females than males (J:76863)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:114480 , J:180385




Genotype
MGI:3720700
tg32
Allelic
Composition
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: C57BL/6 * DBA/2 * SJL * SW
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice display amyloid plaques as early as 6 months, but do become numerous only in older mice (8.5 to 15 months) (J:100965)
• deposits contain both Abeta1-40 and Abeta1-42 peptides (J:100965)
• mice display amyloid plaques as early as 6 months, but do become numerous only in older mice (8.5 to 15 months) (J:100965)
• deposits contain both Abeta1-40 and Abeta1-42 peptides (J:100965)

renal/urinary system
• kidney glomeruli are dilated probably due to obstruction from the amyloid in the lumen or walls of medullary tubules especially in the papilla (J:174270)
• kidney glomeruli are dilated probably due to obstruction from the amyloid in the lumen or walls of medullary tubules especially in the papilla (J:174270)

homeostasis/metabolism
• some mutants older than 18 months exhibit amyloid deposits in the spleen, kidneys, liver, ovary and/or heart (J:174270)
• amyloid is deposited concentrically in the perifollicular sheath, partly or completely encircling the follicles in the spleen (J:174270)
• amyloid replaces most of the splenic red pulp (J:174270)
• in the liver, amyloid deposit is in the walls of sinusoids or central veins (J:174270)
• in the kidney, amyloid deposits are seen in the glomeruli (J:174270)
• amyloid deposits in the heart are not composed of amyloid-beta peptide, but rather amyloid A (J:174270)
• some mutants older than 18 months exhibit amyloid deposits in the spleen, kidneys, liver, ovary and/or heart (J:174270)
• amyloid is deposited concentrically in the perifollicular sheath, partly or completely encircling the follicles in the spleen (J:174270)
• amyloid replaces most of the splenic red pulp (J:174270)
• in the liver, amyloid deposit is in the walls of sinusoids or central veins (J:174270)
• in the kidney, amyloid deposits are seen in the glomeruli (J:174270)
• amyloid deposits in the heart are not composed of amyloid-beta peptide, but rather amyloid A (J:174270)
• mice display amyloid plaques as early as 6 months, but do become numerous only in older mice (8.5 to 15 months) (J:100965)
• deposits contain both Abeta1-40 and Abeta1-42 peptides (J:100965)
• mice display amyloid plaques as early as 6 months, but do become numerous only in older mice (8.5 to 15 months) (J:100965)
• deposits contain both Abeta1-40 and Abeta1-42 peptides (J:100965)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:174270




Genotype
MGI:3722307
tg33
Allelic
Composition
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• transmission of transgene decreases from expected 50% with each backcross generation, suggesting that there is pre-weaning or in utero lethality of transgenic mice; N2 generation mice crossed to (C57BL x SJL)F1 mice show restoration of expected 50% transmission and decreased early mortality (16% vs 36% in N2 generation) (J:43446)
• transmission of transgene decreases from expected 50% with each backcross generation, suggesting that there is pre-weaning or in utero lethality of transgenic mice; N2 generation mice crossed to (C57BL x SJL)F1 mice show restoration of expected 50% transmission and decreased early mortality (16% vs 36% in N2 generation) (J:43446)
• after 1 backcross to C57BL/6 (or N1 generation), 1/3 mice die by <150 days of age; N2 generation mice show 36% lethality with median age at death of ~87 days, while in the N3 generation, 50% mortality is seen at median age of 65 days and in the N4 generation, 100% of mice die with median age of 65 days (J:43446)
• after 1 backcross to C57BL/6 (or N1 generation), 1/3 mice die by <150 days of age; N2 generation mice show 36% lethality with median age at death of ~87 days, while in the N3 generation, 50% mortality is seen at median age of 65 days and in the N4 generation, 100% of mice die with median age of 65 days (J:43446)

behavior/neurological
N
• Background Sensitivity: mice do not show obvious behavioral abnormalities (J:43446)
• Background Sensitivity: mice do not show obvious behavioral abnormalities (J:43446)




Genotype
MGI:3710766
tg34
Allelic
Composition
Tg(APPSWE)2576Kha/0
Genetic
Background
involves: C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(APPSWE)2576Kha mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• at 24 months (J:159623)
• at 24 months (J:159623)
• only occur in forebrain after 6 months of age, and no cerebellar deposits are routinely observed (J:101023)
• only occur in forebrain after 6 months of age, and no cerebellar deposits are routinely observed (J:101023)
• at 2 years (J:121703)
• at 2 years (J:121703)
• at 24 months, mice develop amyloid plaques in the cerebral cortex and hippocampus unlike wild-type mice (J:159623)
• at 24 months, mice develop amyloid plaques in the cerebral cortex and hippocampus unlike wild-type mice (J:159623)
• at 24 months (J:159623)
• at 24 months (J:159623)

cardiovascular system
• after myocardin gene transfer to neocortical pial vessels in 16-month old mice, mice show significant reduction in cerebral blood flow response to whisker stimulation (J:119251)
• after myocardin gene transfer to neocortical pial vessels in 16-month old mice, mice show significant reduction in cerebral blood flow response to whisker stimulation (J:119251)

hematopoietic system
• at 24 months (J:159623)
• at 24 months (J:159623)

immune system
• at 24 months (J:159623)
• at 24 months (J:159623)

homeostasis/metabolism
• formic acid extractable Abeta40 and Abeta42 levels are dramatically elevated at 14.5 months compared to Tg(Prnp-ITM2B/APP695*42)A12Emcg mice (J:101023)
• formic acid extractable Abeta40 and Abeta42 levels are dramatically elevated at 14.5 months compared to Tg(Prnp-ITM2B/APP695*42)A12Emcg mice (J:101023)
• only occur in forebrain after 6 months of age, and no cerebellar deposits are routinely observed (J:101023)
• only occur in forebrain after 6 months of age, and no cerebellar deposits are routinely observed (J:101023)
• at 2 years (J:121703)
• at 2 years (J:121703)
• at 24 months, mice develop amyloid plaques in the cerebral cortex and hippocampus unlike wild-type mice (J:159623)
• at 24 months, mice develop amyloid plaques in the cerebral cortex and hippocampus unlike wild-type mice (J:159623)

Mouse Models of Human Disease
OMIM ID Ref(s)
Alzheimer Disease; AD 104300 J:119251





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last database update
02/02/2016
MGI 6.02
The Jackson Laboratory