Unconventional Slow Virus에 감염된 마우스 뇌조직에서 S100β 단백 mRNA 발현

다국어 초록 (Multilingual Abstract)

Unconventional slow virus induced amyloid plaques formation in mouse brain is very useful animal model for research of Alzheimers disease(AD). The presense of abnormal levels of neurotrophic factors in AD is one possible explanation for the increased concentration of aggregates of over-grown neurites in neuritic plaques of AD. The data presented here demonstrate that the levels of S100p protein and mRNA were greatly elevated in extracts of brain samples of unconventional slow virus infected mice compared to those of control mice. The cells containing the increased S100 p were reactive astrocytes; the amyloid plaques were surrounded by S100p containing astrocytes. A generalization of our finding is that when elevated S100p expression accompanies the gliosis observed in chronic neurodegenerative disease and unconventional slow viurs infection, these will be on associated increase in neurotrophic activity result in abnormal neuritic morphology.