Mouse Genome Informatics
tg
    Tg(PRNP-APPSweInd)8Dwst/0
involves: C3H/HeJ * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
       

Increase in creatine deposits in hippocampus of Tg(PRNP-APPSweInd)8Dwst/0 mice with age

mortality/aging
• Background Sensitivity: 20/52 mice die before 120 days, 3/52 by 130 days and 3/52 die after 250 days; 50% survive for at least a year

behavior/neurological
• mice show impairment in acquisition of spatial information during place discrimination training at 11 weeks of age; mice show longer latencies to reach escape platform and longer search paths to reach platform
• during probe trial after completion of training, mice display lower annulus crossing index, searching for platform in a circular fashion and often crossing the centers of alternative quadrants, relative to non-transgenic controls

nervous system
N
• no differences are seen in volume of dorsal hippocampus or in neuronal cytoarchitecture between transgenic and control mice (J:69967)
• dense-cored amyloid deposits contain amyloid beta-42 peptide (J:69967)
• 14-month old mutants show dense amyloid beta core plaques in the hippocampus (J:166801)
• by 101 days, plaques are detected within the pial vessels, and in the cerebral vasculature by 196 days
• amyloid plaques are associated with dystrophic neurites; dystrophic neuron pathology increases with age and frequency of large cored plaques

homeostasis/metabolism
• increase in creatine deposits in the hippocampal gray matter as mutants age
• potent deposition of cerebral amyloid is observed in all mice 90 days of age
• dense-cored amyloid deposits contain amyloid beta-42 peptide (J:69967)
• 14-month old mutants show dense amyloid beta core plaques in the hippocampus (J:166801)
• by 101 days, plaques are detected within the pial vessels, and in the cerebral vasculature by 196 days

Mouse Models of Human Disease
OMIM IDRef(s)
Alzheimer Disease; AD 104300 J:166801