High levels of circulating β-amyloid peptide do not cause cerebral β-amyloidosis in transgenic mice

摘要: We have established transgenic mice that constitutively overproduce the signal sequence and 99-amino-acid carboxyl-terminal region of human beta-amyloid precursor protein. The strongly expressed transgene in multiple tissues under control a cytomegalovirus enhancer/chick beta-actin promoter. There were exceptionally high levels peptides plasma (approximately 17 times or more compared with level). Although some from one founder line developed amyloidosis intestine, no neuropathology was found up to age 29 months. Given absence cerebral beta-amyloidosis despite extremely circulating mice, results suggest local metabolism protein may play predominant role mice. Such be useful for investigation etiology disease establishment therapeutic strategies.