General Information

Transgene: Double transgenic PS2APP mice were bred by crossing homozygous APPswe (line 71) males with PS2_mut (line 30) females

Mutation: APP (K670N, M671L) and PS2 (N141I)

Promoter: Murine prion protein genomic fragment (pPrnpHG) was used for PS2mThy-1.2 for APPSw

Origin: (C57BL/6xDBA/2)

Phenotype

Neuropathological analysis:

At 8 months, PS2APP mice develop age-related cognitive deficits and correlative amyloid deposits with inflammation in neo- and limbic cortices, including the hippocampal formation and amygdala, as well as thalamic and pontine nuclei. The metabolic profile showed clear indication of hypometabolism with age (20m) in the PS2APP mice: both N-acetyl-aspartate and glutamate were significantly reduced in the older animals. These spectroscopic measures in vivo correlated well with the plaque load in the frontal cortex.

Behavioral:

Behavioral changes begin when Aß deposits and inflammation appear in the subiculum and frontolateral cortex.

Availability

Laurence Ozmen
F. Hoffmann-La Roche AG
Building 69/440 Grenzacherstr 124, CH-4070
Basel, Switzerland
Phone: +41 61 6870248
Fax: +41 61 688 4575
Email: Laurence.ozmen@roche.com

Reference

Primary:

J.G. Richards, G.A. Higgins, A.M. Ouagazzal, L. Ozmen, J.N. Kew, B. Bohrmann, P. Malherbe, M. Brockhaus, H. Loetscher, C. Czech, G. Huber, H. Bluethmann, H. Jacobsen and J.A. Kemp. PS2APP transgenic mice, coexpressing hPS2mut and hAPPswe, show age-related cognitive deficits associated with discrete brain amyloid deposition and inflammation, J. Neurosci. 23:8989-9003, 2003. Abstract.

Associated:

von Kienlin M, Künnecke B, Metzger F, Steiner G, J. Richards G, Ozmen L, Jacobsen H, Loetscher H. Altered metabolic profile in the frontal cortex of PS2APP transgenic mice, monitored throughout their life span. Neurobiology of Dis. 18(1):32-39, 2005. Abstract.