Mouse Genome Informatics
cx1
    Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr/0
Tg(Thy1-MAPT*P301S)2541Godt/0

B6.Cg-Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr Tg(Thy1-MAPT*P301S)2541Godt
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• at 12 months, mice exhibit a 3- to 4-fold increase in Tau lesions compared with Tg(Thy1-MAPT*P301S)2541Godt mice


Mouse Genome Informatics
cx2
    Tg(Prnp-ITM2B*)7Jckr/0
Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr/0

C57BL/6-Tg(Prnp-ITM2B*)7Jckr Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• mice exhibit a 68% reduction in neocortical amyloid beta deposition compared with Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice

homeostasis/metabolism
• mice exhibit an accumulation of Dan-amyloid in separate plaques from amyloid beta plaques
• mice exhibit a 68% reduction in neocortical amyloid beta deposition compared with Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice


Mouse Genome Informatics
cx3
    Abcb1atm1Bor/Abcb1atm1Bor
Abcb1btm1Bor/Abcb1btm1Bor
Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr/0

FVB.Cg-Abcb1btm1Bor Abcb1atm1Bor Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• mutants exhibit an increase in the cortical load and size of amyloid beta-positive plaques compared to single Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice

homeostasis/metabolism
• mutants exhibit an increase in the cortical load and size of amyloid beta-positive plaques compared to single Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice


Mouse Genome Informatics
cx4
    Abcc1tm1Bor/Abcc1tm1Bor
Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr/0

FVB.Cg-Abcc1tm1Bor Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• increase in microgliosis
• mutants exhibit an increase in the cortical load and size of cerebral amyloid beta-positive plaques compared to single Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice

hematopoietic system
• increase in microgliosis

immune system
• increase in microgliosis

homeostasis/metabolism
• mutants exhibit an increase in the cortical load and size of cerebral amyloid beta-positive plaques compared to single Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr mice

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:178230


Mouse Genome Informatics
cx5
    Abcg2tm1Ahs/Abcg2tm1Ahs
Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr/0

FVB.Cg-Abcg2tm1Ahs Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• mutants exhibit a similar amount of cortical amyloid beta-positive plaques as seen in single Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr transgenic mice

homeostasis/metabolism
• mutants exhibit a similar amount of cortical amyloid beta-positive plaques as seen in single Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr transgenic mice


Mouse Genome Informatics
tg6
    Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr/0
C57BL/6-Tg(Thy1-APPSw,Thy1-PSEN1*L166P)21Jckr
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• mutants develop amyloid plaques over time that increase in size, with the highest rate of new plaque appearance in mice between 4 and 5 months of age
• newly formed plaques and preexisting plaques grow at similar rates

homeostasis/metabolism
• mutants develop amyloid plaques over time that increase in size, with the highest rate of new plaque appearance in mice between 4 and 5 months of age
• newly formed plaques and preexisting plaques grow at similar rates

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:180835