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

Ken Ichiro Fukuchi, Libin Ho, Steven G. Younkin, Dennis D. Kunkel, Charles E. Ogburn, Renee C. LeBoeuf, Clement E. Furlong, Samir S. Deeb, David Nochlin, Jerzy Wegiel, Henry M. Wisniewski, George M. Martin

Research output: Contribution to journalArticlepeer-review

66 Scopus citations


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

Original languageEnglish (US)
Pages (from-to)219-227
Number of pages9
JournalAmerican Journal of Pathology
Issue number1
StatePublished - Jul 1996

ASJC Scopus subject areas

  • Pathology and Forensic Medicine


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