Mouse Genome Informatics
cx1
    Apoetm1Unc/Apoetm1Unc
Tg(GFAP-APOE_i4)#Hol/0

B6.Cg-Apoetm1Unc Tg(GFAP-APOE_i4)#Hol
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
behavior/neurological
• mice require more time to habituate to a novel environment compared to wild-type mice
• at 14 to 17 months of age, mice did not perform as well as Apoetm1Unc homozygotes and Tg(GFAP-APOE_i3)37Hol Apoetm1Unc/Apoetm1Unc mice in a rotating holeboard test
• however, mice perform as well as wild-type mice in a rotating holeboard test
• mice exhibit an impairment in working memory in a radial arm maze test compared to wild-type mice
• compared to wild-type mice
• mice spend less time than wild-type mice and Apoetm1Unc homozygotes in the center of an open field
• mice exhibit increased numbers of fine movement (not related to ambulation) compared to wild-type mice


Mouse Genome Informatics
cx2
    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)