Mouse Genome Informatics
cx1
    Tg(APPSWE)2576Kha/0
Tg(Prnp-ITM2B/APP695*42)A12Emcg/0

involves: C3H * C57BL/6 * SJL
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• mice show enhanced senile plaque pathology in the forebrain at 14.5 months
• mice show elevated insoluble Abeta levels in the hindbrain at 14.5 months
• 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

other phenotype
• 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
• 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


Mouse Genome Informatics
tg2
    Tg(Prnp-ITM2B/APP695*42)A12Emcg/0
involves: C3H * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
• forebrain pathology only consistently develops after 12 months of age
• reactive gliosis is associated with plaques
• cored plaques can be observed as early as 3 months in molecular layer of cerebella of transgenic mice and becoming more pronounced with age; occasional extracellular plaques are seen in the entorhinal/piriform cortices and hippocampus at 6 months of age, but aren't consistently found until >12 months of age
• oldest mice show widespread pathology with cored and diffuse plaques in cerebellum, cortex, hippocampus, and olfactory bulb
• extracellular amyloid plaques show dense amyloid cores with radiating fibrils; many bundles of dystrophic neurites are observed at the periphery of these plaques
• compact plaques range from 38 um in diameter at 3 months to 58 um at 1-18 months
• tau pathology is not evident
• endogenous mouse Abeta is detected in some cored plaques and in diffuse deposits in older mice

other phenotype
• Abeta1-42 peptide levels in 3-month old transgenic brains are ~1- to 1.5-fold higher than levels in 3- and 6-month oldTg(APPSWE)2576Kahs controls
• cored plaques can be observed as early as 3 months in molecular layer of cerebella of transgenic mice and becoming more pronounced with age; occasional extracellular plaques are seen in the entorhinal/piriform cortices and hippocampus at 6 months of age, but aren't consistently found until >12 months of age
• oldest mice show widespread pathology with cored and diffuse plaques in cerebellum, cortex, hippocampus, and olfactory bulb
• extracellular amyloid plaques show dense amyloid cores with radiating fibrils; many bundles of dystrophic neurites are observed at the periphery of these plaques
• compact plaques range from 38 um in diameter at 3 months to 58 um at 1-18 months
• tau pathology is not evident
• endogenous mouse Abeta is detected in some cored plaques and in diffuse deposits in older mice

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:101023