Mouse Genome Informatics
cn1
    Gsk3atm1.1Tac/Gsk3atm1.1Tac
Tg(APPV717F)109Ili/0
Tg(Camk2a-cre)#Stl/0

involves: BALB/c * C57BL * C57BL/6NTac
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• significant decrease in amyloid beta senile plaques compared to transgenic mice wild-type for Gsk3a

behavior/neurological
N
• performance in a Barnes maze and in an open field are similar to wild-type controls unlike transgenic mice wild-type for Gsk3a (J:184975)

homeostasis/metabolism
• significant decrease in amyloid beta senile plaques compared to transgenic mice wild-type for Gsk3a


Mouse Genome Informatics
cx2
    Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili

involves: 129P2/OlaHsd
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex
• deposits are diffuse in appearance; deposition is prominent in dentate hilus, but little or none in molecular layer of dentate gyrus
• at 12 months, mice have high levels of insoluble Abeta42
• at 3 months, cerebral spinal fluid levels of Abeta40 and Abeta42 are elevated; Abeta40 increase is greater than in transgenic, Apoe-single null animals

homeostasis/metabolism
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex
• deposits are diffuse in appearance; deposition is prominent in dentate hilus, but little or none in molecular layer of dentate gyrus
• at 12 months, mice have high levels of insoluble Abeta42
• at 3 months, cerebral spinal fluid levels of Abeta40 and Abeta42 are elevated; Abeta40 increase is greater than in transgenic, Apoe-single null animals

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:107702


Mouse Genome Informatics
cx3
    Apoetm1Unc/Apoetm1Unc
Clutm1Jakh/Clutm1Jakh
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili

involves: 129P2/OlaHsd * 129S2/SvPas
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• at 6 months of age, most mice have substantial amyloid beta (Abeta) deposits
• by 12 months of age, mice have more amyloid beta (Abeta) deposits in the hippocampus and cortex than other genotypes
• Abeta deposits are more numerous and fill all parts of hippocampus and some of the cortex by 12 months; abundant compact and diffuse plaques are observed
• mice have greater levels of thioflavine-S-positive (fibrillar) Abeta deposits than other genotypes, similar to transgenic homozygotes with normal Apoe and Clu
• at 3 months, cerebral spinal fluid levels of Abeta40 and Abeta42 are elevated

homeostasis/metabolism
• mice have significant amyloid burden, greater than shown by other genotypes
• at 12 months, mice have highest tissue levels of soluble Abeta40 and Abeta42, with high levels of insoluble Abeta42
• at 3 months, mice have higher levels of carbonate soluble Abeta40 and Abeta42 compared to other genotypes
• at 6 months of age, most mice have substantial amyloid beta (Abeta) deposits
• by 12 months of age, mice have more amyloid beta (Abeta) deposits in the hippocampus and cortex than other genotypes
• Abeta deposits are more numerous and fill all parts of hippocampus and some of the cortex by 12 months; abundant compact and diffuse plaques are observed
• mice have greater levels of thioflavine-S-positive (fibrillar) Abeta deposits than other genotypes, similar to transgenic homozygotes with normal Apoe and Clu
• at 3 months, cerebral spinal fluid levels of Abeta40 and Abeta42 are elevated

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:107702


Mouse Genome Informatics
cx4
    Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0

involves: 129P2/OlaHsd * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• 40% of mice exhibit plaque depositions at 12 months of age with one mouse remaining plaque free at 21 months (J:127846)
• 23% of mice at 15 months, 33% at 18 months and 55% at 21 months exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)
• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus (J:127846)
• 3 of 4 mice exhibit plaques by 12 months of age (J:133058)

homeostasis/metabolism
• 40% of mice exhibit plaque depositions at 12 months of age with one mouse remaining plaque free at 21 months (J:127846)
• 23% of mice at 15 months, 33% at 18 months and 55% at 21 months exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)
• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus (J:127846)
• 3 of 4 mice exhibit plaques by 12 months of age (J:133058)


Mouse Genome Informatics
cx5
    Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i4)#Hol/0

involves: 129P2/OlaHsd * C57BL/6 * CBA
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• by 15 to 18 months, 60% of mice exhibit plaques in the hippocampus (J:127846)
• the amount of amyloid deposited is more than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc mice but much less than in Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:127846)
• plaques are observed in the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)
• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)
• 55.6% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)
• mice exhibit increased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc mice (J:133058)
• 44% of mice exhibit thioflavine-S+ amyloid staining (fibrillar amyloid) in the molecular layer unlike in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc and Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:133058)

homeostasis/metabolism
• by 15 to 18 months, 60% of mice exhibit plaques in the hippocampus (J:127846)
• the amount of amyloid deposited is more than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc mice but much less than in Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:127846)
• plaques are observed in the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)
• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gyrus (J:127846)
• 55.6% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)
• mice exhibit increased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc mice (J:133058)
• 44% of mice exhibit thioflavine-S+ amyloid staining (fibrillar amyloid) in the molecular layer unlike in Tg(APPV717F)109Ili Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc and Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:133058)


Mouse Genome Informatics
cx6
    Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i3)37Hol/0

involves: 129P2/OlaHsd * C57BL/6 * CBA
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• by 15 to 18 months, 31% of mice exhibit plaques in the hippocampus (J:127846)
• the amount of amyloid deposited is less than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and much less than in Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:127846)
• plaques are observed in the the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)
• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gurys (J:127846)
• 20% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)
• mice exhibit decreased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc mice (J:133058)

homeostasis/metabolism
• by 15 to 18 months, 31% of mice exhibit plaques in the hippocampus (J:127846)
• the amount of amyloid deposited is less than in Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc and much less than in Tg(APPV717F)109Ili Apoetm1Unc/Apoetm1Unc mice (J:127846)
• plaques are observed in the the outer molecular layer of the dentate gyrus and the stratum oriens and radiatum of the hippocampus (J:127846)
• mice exhibit fibrillar plaques in the outer molecular layer of the dentate gurys (J:127846)
• 20% of mice exposed to traumatic brain injury (TBI) at 9 to 10 months of age exhibit amyloid plaques by 12 to 13 months of age while mice not exposed to TBI do not exhibit plaques until 15 months of age (J:133058)
• mice exhibit decreased plaque formation and severity following TBI compared to in similarly treated Tg(APPV717F)109Ili Tg(GFAP-APOE_i4)#Hol Apoetm1Unc/Apoetm1Unc mice (J:133058)


Mouse Genome Informatics
cx7
    Apoetm1Unc/Apoetm1Unc
Tg(APPV717F)109Ili/0
Tg(GFAP-APOE_i2)14Hol/0

involves: 129P2/OlaHsd * C57BL/6 * CBA
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• 66% of mice exhibit plaques after 18 months
• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus but no the molecular layer of the dentate gyrus
• however, no fibrillar plaques are detected

homeostasis/metabolism
• 66% of mice exhibit plaques after 18 months
• mice exhibit plaques in the stratum oriens and radiatum of the hippocampus and hilus of the dentate gyrus but no the molecular layer of the dentate gyrus
• however, no fibrillar plaques are detected


Mouse Genome Informatics
cx8
    Clutm1Jakh/Clutm1Jakh
Tg(APPV717F)109Ili/Tg(APPV717F)109Ili

involves: 129S2/SvPas
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition (J:78357)
• decreased percentage of Abeta-immunoreactive deposits that are thioflavine-S-positive (2.46 vs 19.4% thioflavine load/Abeta load) compared to Clu-sufficient mice (J:78357)
• many Abeta deposits have few or no detectable dystrophic neurites around them (J:78357)
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex (J:107702)
• a 10-fold reduction in dystrophic neurites in hippocampi at 12 months compared to Clu-sufficient transgenic mice and a 5-fold reduction in number of dystrophic neurites per amyloid deposit

homeostasis/metabolism
• only 20% of mice have thioflavine-S-positive (fibrillar Abeta or amyloid) deposits in the cortex at 12 months
• mice have lower hippocampal amyloid burden (0.89%) at 12 months than Clu-sufficient transgenic mice; amyloid load increases to 2.25% by 15 months
• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition (J:78357)
• decreased percentage of Abeta-immunoreactive deposits that are thioflavine-S-positive (2.46 vs 19.4% thioflavine load/Abeta load) compared to Clu-sufficient mice (J:78357)
• many Abeta deposits have few or no detectable dystrophic neurites around them (J:78357)
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex (J:107702)

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:78357


Mouse Genome Informatics
cx9
    Lrpap1tm1Her/Lrpap1tm1Her
Tg(APPV717F)109Ili/0

involves: 129S7/SvEvBrd * C57BL/6 * DBA/2
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• elevated amyloid deposits over controls
• develop reactive astrocytosis

homeostasis/metabolism
• elevated amyloid deposits over controls


Mouse Genome Informatics
cx10
    Msr1tm1Csk/Msr1tm1Csk
Tg(APPV717F)109Ili/?

involves: 129X1/SvJ * C57BL/6 * DBA/2 * ICR
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• number and distribution of plaques was similar to those seen in wild-type (Msr1+) mice heterozygous for Tg(APP)109Ili
• loss of synaptophysin-immunoreactive presynaptic terminals in the hippocampal outer molecular layer (loss was similar to that seen in wild-type (Msr1+) mice heterozygous for Tg(APP)109Ili )
• reduced density of MAP-2 immuoreactive neuronal dendrites in the outer molecular layer of the hippocampus (loss was similar to that seen in wild-type (Msr1+) mice heterozygous for Tg(APP)109Ili)

homeostasis/metabolism
• number and distribution of plaques was similar to those seen in wild-type (Msr1+) mice heterozygous for Tg(APP)109Ili

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:58338


Mouse Genome Informatics
cx11
    Tg(APPV717F)109Ili/0
Tg(Prnp-MAPT*P301S)PS19Vle/0

involves: C3H * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• median survival of females and males is 12 and 10 months of age, respectively
• mutants exhibit a greater acceleration of death than single Tg(Prnp-MAPT*P301S)PS19Vle mice

growth/size
• decrease in weight with increasing age
• males show a greater decrease in percentage of body weight than females
• mutants exhibit a greater acceleration weight loss than single Tg(Prnp-MAPT*P301S)PS19Vle mice

behavior/neurological
• 56% of mutants exhibit paresis or paralysis and presence of a hunchback posture at 11 months of age
• males show a more profound motor phenotype than females
• mutants exhibit a greater acceleration of motor phenotype than single Tg(Prnp-MAPT*P301S)PS19Vle mice
• 56% of mutants exhibit paresis or paralysis and presence of a hunchback posture at 11 months of age

nervous system
• limited amyloid beta deposits are seen at 8 months of age within the corpus callosum, stratum oriens, and radiatum of CA1, visual cortex, molecular layer of the dentate gyrus, and retrosplenial area
• at 11 months of age, an increase in amyloid beta deposition is seen in the same areas as at 8 months of age
• mutants exhibit an increase in plaque load with increasing age from 8 to 11 months of age for the anterior and posterior hippocampus
• most amyloid beta deposits are not composed of amyloid beta species that are assembled into ThS-positive amyloid fibrils
• mutants develop ThS-positive neurofibrillary tangles at a much earlier age than single Tg(Prnp-MAPT*P301S)PS19Vle mice
• a greater proportion of double mutants develop tangles at 8 and 11 months of age than single Tg(Prnp-MAPT*P301S)PS19Vle mice
• mutants exhibit an accelerated progression in the distribution of abnormally phosphorylated tau from the entorhinal and neocortex, followed by involvement of the hippocampal formation and subcortical structures, to finally penetration of all layers of the neocortex compared to single Tg(Prnp-MAPT*P301S)PS19Vle mice
• substantial loss of neurons that secrete amyloid beta

skeleton
• 56% of mutants exhibit paresis or paralysis and presence of a hunchback posture at 11 months of age

homeostasis/metabolism
• limited amyloid beta deposits are seen at 8 months of age within the corpus callosum, stratum oriens, and radiatum of CA1, visual cortex, molecular layer of the dentate gyrus, and retrosplenial area
• at 11 months of age, an increase in amyloid beta deposition is seen in the same areas as at 8 months of age
• mutants exhibit an increase in plaque load with increasing age from 8 to 11 months of age for the anterior and posterior hippocampus
• most amyloid beta deposits are not composed of amyloid beta species that are assembled into ThS-positive amyloid fibrils

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:165441


Mouse Genome Informatics
cx12
    Tg(APPV717F)109Ili/0
Tg(Prnp-Abca1)EHol/0

involves: C57BL/6 * CBA
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• at 12 months, rare amyloid beta (Abeta) deposits are observed in the cortex, with occasional deposits in the molecular layer of hippocampus and frequent Abeta deposits in the hilus of the dentate gyrus; mice show 3-fold less Abeta in the brain relative to Tg(APPV717F)109Ili, Abca1-wild-type controls
• fibrillar Abeta plaques are frequently observed in cortex and hippocampus
• Abeta deposits are almost all diffuse, with little true amyloid
• very few clusters of reactive microglia are seen in brain

homeostasis/metabolism
• at 12 months, rare amyloid beta (Abeta) deposits are observed in the cortex, with occasional deposits in the molecular layer of hippocampus and frequent Abeta deposits in the hilus of the dentate gyrus; mice show 3-fold less Abeta in the brain relative to Tg(APPV717F)109Ili, Abca1-wild-type controls
• fibrillar Abeta plaques are frequently observed in cortex and hippocampus
• Abeta deposits are almost all diffuse, with little true amyloid
• very few clusters of reactive microglia are seen in brain


Mouse Genome Informatics
tg13
    Tg(APPV717F)109Ili/Tg(APPV717F)109Ili
Not Specified
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition (J:78357)
• mice have a higher percentage of thioflavine-S positive Abeta-immunoreactive deposits than Clu-null mice (J:78357)
• all deposits are surrounded by multiple enlarged, dystrophic neurites (J:78357)
• a 2-fold increase in monomeric Abeta is detected in the brain compared to Clu-deficient transgenic mice (J:78357)
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex (J:107702)
• mice have prominent deposits that are both diffuse and compact in appearance in hippocampus and in molecular layer of dentate gyrus (J:107702)
• dystrophic neurites are 10-fold higher compared to Clu-null transgenic mice and more dystrophic neurites (5-fold) are associated with each amyloid deposit

homeostasis/metabolism
• 77% of mice have thioflavine-S-positive (fibrillar Abeta or amyloid) deposits in the cortex
• hippocampal amyloid burden is greater (2.76%) than in Clu-null transgenics at 12 months of age
• by 12 months of age, ~60% of mice show amyloid beta (Abeta) deposition (J:78357)
• mice have a higher percentage of thioflavine-S positive Abeta-immunoreactive deposits than Clu-null mice (J:78357)
• all deposits are surrounded by multiple enlarged, dystrophic neurites (J:78357)
• a 2-fold increase in monomeric Abeta is detected in the brain compared to Clu-deficient transgenic mice (J:78357)
• by 12 months of age, mice have amyloid beta (Abeta) deposits in the hippocampus and cortex (J:107702)
• mice have prominent deposits that are both diffuse and compact in appearance in hippocampus and in molecular layer of dentate gyrus (J:107702)

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:78357


Mouse Genome Informatics
tg14
    Tg(APPV717F)109Ili/0
involves: BALB/c * C57BL * C57BL/6NTac
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system

behavior/neurological
• significant deficits in latency to find the target on the Barnes maze and use a poor maze strategy
• increase in locomotor activity in an open field

homeostasis/metabolism

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:184975


Mouse Genome Informatics
tg15
    Tg(APPV717F)109Ili/0
involves: C57BL/6 * DBA/2 * Swiss Webster
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
N
• mice do not show neuronal loss in the hippocampal regions compared to Tg(PDGFB-APP*V717F)H6Lms mice (J:100974)


Mouse Genome Informatics
tg16
    Tg(APPV717F)109Ili/0
Not Specified
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• deposits of human beta-amyloid are seen in the hippocampus, corpus callosum and cerebral cortex, beginning at 6 - 9 months, and increasing in density with age (J:23080)
• mice develop plaques by 12 months of age in the hippocampus and the outer molecular layer of the dentate gyrus with a subset of plaques positive for fibrillar amyloid (J:127846)
• plaque deposition increases with age with greater than 85% of the hippocampus covered in plaques at 24 months of age (J:127846)
• synaptic and dendritic density are reduced in the molecular layer
• amyoid plaques are associated with distorted neurites
• the majority of amyloid plaques are surrounded by GFAP-positive reactive astrocytes

homeostasis/metabolism
• deposits of human beta-amyloid are seen in the hippocampus, corpus callosum and cerebral cortex, beginning at 6 - 9 months, and increasing in density with age (J:23080)
• mice develop plaques by 12 months of age in the hippocampus and the outer molecular layer of the dentate gyrus with a subset of plaques positive for fibrillar amyloid (J:127846)
• plaque deposition increases with age with greater than 85% of the hippocampus covered in plaques at 24 months of age (J:127846)

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:23080