Modification: APP: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: N/A
Genetic Background: C57BL/6 x DBA/2
Availability: Available through Ken-ichiro Fukuchi, University of Illinois College of Medicine at Peoria
Transgene consisting of the signal plus 99-amino acid carboxyl-terminal sequence (SbC) of human APP under the control of a cytomegalovirus enhancer/β-actin promoter.
Although the transgene is expressed in brain and skeletal muscle, no neuropathology was found in transgenic mice up to age 29 months (Fukuchi et al., 1996). Pathology reminiscent of inclusion body myopathy observed at 6-12 months: Aβ-immunoreactive deposits in skeletal muscle fibers. Muscle fibers with Aβ-immunoreactive deposits increased with age and also became vacuolated (Fukuchi et al., 1998).
Hypoactivity. The acquisition of place learning in the Morris water maze task was impaired (Lalonde et al., 2002).
Available through Ken-ichiro Fukuchi.
- Fukuchi K, Ho L, Younkin SG, Kunkel DD, Ogburn CE, Leboeuf RC, Furlong CE, Deeb SS, Nochlin D, Wegiel J, Wisniewski HM, Martin GM. High levels of circulating beta-amyloid peptide do not cause cerebral beta-amyloidosis in transgenic mice. Am J Pathol. 1996 Jul;149(1):219-27. PubMed.
- Fukuchi K, Pham D, Hart M, Li L, Lindsey JR. Amyloid-beta deposition in skeletal muscle of transgenic mice: possible model of inclusion body myopathy. Am J Pathol. 1998 Dec;153(6):1687-93. PubMed.
- Lalonde R, Dumont M, Fukuchi K, Strazielle C. Transgenic mice expressing the human C99 terminal fragment of betaAPP: effects on spatial learning, exploration, anxiety, and motor coordination. Exp Gerontol. 2002 Dec;37(12):1401-12. PubMed.
- Strazielle C, Dumont M, Fukuchi K, Lalonde R. Transgenic mice expressing the human C99 terminal fragment of betaAPP: effects on cytochrome oxidase activity in skeletal muscle and brain. J Chem Neuroanat. 2004 Jul;27(4):237-46. PubMed.
No Available Further Reading