Posted 29 July 2010
Transgene: Human K369I mutant tau cDNA, lacking exon 3 and containing four MT-binding domains, was cloned together with a Kozak consenus seq. into a murine Thy1.2 expression vector.
Mutation: Tau K369I
Promoter: Murine Thy 1.2
Mouse strain: B6D2F1xB6D2F1
Neuropathological Analysis:
Early onset memory impairment and FTD-assoc. Parkinson. K369I expressed in cortex, hippocampus, basal ganglia and substantia nigra. Forbrain levels 2.9 higher than WT.
Behavioral:
Early-onset (four weeks) motor phenotype of Parkinsonism with tremor, bradykinesia, abnormal gait and postural instability. Symptoms partially reversible with L-dopa in early stages.
Lars Ittner or Jürgen Götz
Alzheimer’s and Parkinson’s Disease Lab, Brain and Mind Res. Institute
University of Sydney, Camperdown,, NSW 2050, Australia
E-mail: Jürgen Götz (juergen.goetz@sydney.edu.au) and Lars Ittner (lars.ittner@sydney.edu.au)
Patents: None
Primary:
Ittner LM, Fath T, Ke YD, Bi M, van Eersel J, Li KM, Gunning P, Götz J. Parkinsonism and impaired axonal transport in a mouse model of frontotemporal dementia. Proc Natl Acad Sci U S A. 2008 Oct 14;105(41):15997-6002. Abstract
Associated:
Van Eersel J, Ke YD, Liu X, Delerue F, Kril JJ, Götz J, Ittner LM. Sodium selenate mitigates tau pathology, neurodegeneration, and functional deficits in Alzheimer's disease models. Proc Natl Acad Sci U S A. 2010 Jul 19. Abstract
Ittner LM, Ke YD, Götz J. Phosphorylated Tau interacts with c-Jun N-terminal kinase-interacting protein 1 (JIP1) in Alzheimer disease. J Biol Chem. 2009 Jul 31;284(31):20909-16. Abstract
|
Home
