Abstract
Alzheimer’s disease (AD), a neurodegenerative disorder that severely impairs cognitive and memory function in elderly people, is partially characterized neuropathologically by extracellular deposits of β-amyloid protein. We were interested in studying how β-amyloid may be involved in aspects of AD pathogenesis. To do this, we expressed the last 100 amino acids of the amyloid precursor protein, which contains the entire β-amyloid region, in PC12 cells and in brains of transgenic mice. We found that expression of this fragment of βPP altered cytoskeletal changes in PC12 cells following nerve growth factor treatment. Using both in vitro and in vivo systems of human βPP expression, we can study the biology of βPP and test hypotheses of how it may be involved in Alzheimer’s disease.
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