Posted 26 July 2005

General Information

Transgene: Crossed APPV717I (London) with PS1 (n-/-).

Mutation: APP V717I (London)

Promoter: Thy 1

Mouse strain: FVB/N (Crl)

Phenotype

Neuropathological Analysis:

In bigenic mice the neuronal absence of PS1 effectively prevented amyloid pathology, even in mice that were 18 months old, whereas single APP (V717I) mice develop amyloid pathology at 10-12 months. LTP also was rescued in bigenic mice but not the cognitive defect of APP(V717I) mice.

Behavioral

normal

Availability

Mice can be made available for academic collaboration under MTA with KULeuven-R&D. For information on these mice, please contact:

Paul Van Dun
Director - KULeuvenR&D
Groot Begijnhof 59
B-3000 Leuven Belgium
tel +32 16 326508
fax +32 16 326515
Email: Paul.Vandun@lrd.kuleuven.ac.be
Web site: http://www.kuleuven.ac.be/lrd

References

Primary:

Dewachter I, Reversé D, Caluwaerts N, Ris L, Kuipéri C, Van den Haute C, Spittaels K, Umans L, Serneels L, Thiry E, Moechars D, Mercken M, Godaux E, Van Leuven F. Neuronal deficiency of presenilin 1 inhibits amyloid plaque formation and corrects hippocampal long-term potentiation but not a cognitive defect of amyloid precursor protein [V717I] transgenic mice. J Neurosci. 2002 May 1 ; 22(9):3445-53. Abstract

Associated:

Van Dorpe J, Smeijers L, Dewachter I, Nuyens D, Spittaels K, Van Den Haute C, Mercken M, Moechars D, Laenen I, Kuiperi C, Bruynseels K, Tesseur I, Loos R, Vanderstichele H, Checler F, Sciot R, Van Leuven F. Prominent cerebral Amyloid Angioplathy in APP/London transgenic mice. Am J Pathol (2000) 157:1283-1298. Abstract

Moechars D, Dewachter I, Lorent K, Reversé D, Baekelandt V, Naidu A, Tesseur I, Spittaels K, Haute CV, Checler F, Godaux E, Cordell B, Van Leuven F. Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain. J Biol Chem. 1999; 274 (10): 6483-92. Abstract.

Ris L, Dewachter I, Reverse D, Godaux E, Van Leuven F. Capacitative calcium entry induces hippocampal long term potentiation in the absence of presenilin-1. J Biol Chem. 2003; 278(45):44393-9. Abstract.