Mouse Genome Informatics
cx
    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
• 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
• 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)

other phenotype
• 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