Updated 14 April 2005

General Information

Transgene: Human wild-type αSYN was first subcloned into the XhoI site of a modified intermediate vector derived from pNEB193. This construct was digested with AscI and PacI, and the insert was subcloned into an OL-specific proteolipid protein promoter (PLP) cassette that was modified to contain a multiple cloning site after the 3' boundary of intron 1. A linear ApaI-SacII fragment of 11 kb comprising the transgene without plasmid sequences was isolated and injected into C57Bl/6 DBA/2 fertilized oocytes

Promoter: Proteolipid protein promotor

Mouse Strain: C57BL/6. Backcrossed to generation N5

Phenotype

Neuropathological Analysis:

Transgenic αSYN was detected in brain white matter and oligodendrocytes bodies but no other brain cell type. It was detergent insoluble. Hyperphosphorylation at S129 of αSyn in the tg mice.

Availability

Philipp Kahle
Lab of Alzheimer's and Parkinson's Disease Res, Dept Biochemisty
Ludwig Maximilians University of Munich
Schillerstrasse 44, 80336, Munich, Germany
(+49-89) 5996-480, 475
(+49-89) 5996-415
Email: pkahle@pbm.med.uni-muenchen.de

Patents:

References

Primary:

Kahle PJ, Neumann M, Ozmen L, Muller V, Jacobsen H, Spooren W, Fuss B, Mallon B, Macklin WB, Fujiwara H, Hasegawa M, Iwatsubo T, Kretzschmar HA, Haass C. Hyperphosphorylation and insolubility of alpha-synuclein in transgenic mouse oligodendrocytes. EMBO Rep. 2002 Jun 1 ; 3(6):583-8. Abstract

Associated:

Stefanova N, Reindl M, Neumann M, Haass C, Poewe W, Kahle PJ, Wenning GK. Oxidative stress in transgenic mice with oligodendroglial alpha-synuclein overexpression replicates the characteristic neuropathology of multiple system atrophy. Am J Pathol. 2005 Mar;166(3):869-76. Abstract