Regulatory region of human amyloid precursor protein (APP) gene promotes neuron-specific gene expression in the CNS of transgenic mice.

摘要: The accumulation of beta-amyloid protein in specific brain regions is a central pathological feature Alzheimer's disease (AD). 4 kd derives from larger amyloid precursor (APP) by as yet unknown mechanisms. In the absence laboratory animal model AD, transgenic mice expressing various APP gene products may provide new insights into relationship between and formation pathogenesis AD. AD result interactions other molecules. Such are likely to be developmentally regulated tissue-specific. A mouse therefore, would aim for transgene expression that mimics endogenous gene. As an initial step developing model, we have identified 4.5 kb DNA fragment 5' end human gene, which mediates neuron-specific CNS mice, using E. coli lacZ reporter Detectable levels found most neurons but not glial vascular endothelial cells. pattern this closely resembles distribution mRNA both CNS.