General Information

Transgene: Human βAPP cDNA carboxy terminal 99 a.a. and βAPP signal peptide (without AD-specific mutations)

Mutation: none

Promoter: cytomegalovirus enhancer/chicken β-actin

Mouse Strain: B6C3F1 x C57BL/6N hybrid

Phenotype

Neuropathological Analysis:

Accumulation of human Aβ at very high level in pancreas (8600 pmol/g) and in lesser, though readily detectable, amounts in brain (4.1 pmol/g) and kidney (15.0 pmol/g).

Little correlation between Aβ accumulation and the expression of transgenic mRNA because Aβ was not detected in tissues such liver and heart which expressed more transgenic mRNA than pancreas, brain, or kidney.

Accumulation of human Aβ in transgenic plasma in an amount over 30 times that in normal human plasma.

Putative amyloid fibrils in pancreas both in acinar cells and in interstitial macrophages. Like amyloid fibrils in the AD brain, these fibrils had a diameter of 7-12 nm and were stained by anti-Aβ antibody.

Behavioral:

N/A

Availability

Patents: None

Reference

Primary:

Kawarabayashi T, Shoji M, Sato M, Sasaki A, Ho L, Eckman CB, Prada C-M, Younkin SG, Kobayashi T, Norihiro T, Matsubara E, Iizuka T, Harigaya Y, Kasai K, Hirai S. Accumulation of β-amyloid fibrils in pancreas of transgenic mice. Neurobiol Aging. 1996;17(2):215-22. Abstract .

Associated:

Shoji M, Kawarabayashi T, Sato M, Sasaki A, Saido TC, Matsubara E, Tomidokoro Y, Kanai M, Shizuka M, Ishiguro K, Ikeda M, Harigaya Y, Okamoto K, Hirai S. Age-related amyloid β protein accumulation induces cellular death and macrophage activation in transgenic mice. J Pathol 2000 May;191(1):93-101. Abstract.

Shoji M, Kawarabayashi T, Sato M, Sasaki A, Matsubara E, Igeta Y, Kanai M, Tomidokoro Y, Shizuka M, Ishiguro K, Harigaya Y, Okamoto K, Hirai S. Accumulation of amyloid β protein in transgenic mice. Neurobiol Aging 1998 Jan-Feb;19(1 Suppl):S59-63. Abstract .