Conditional transgenic mice expressing C-terminally truncated human α-synuclein (αSyn119) exhibit reduced striatal dopamine without loss of nigrostriatal pathway dopaminergic neurons

@article{Daher2009ConditionalTM,
  title={Conditional transgenic mice expressing C-terminally truncated human α-synuclein (αSyn119) exhibit reduced striatal dopamine without loss of nigrostriatal pathway dopaminergic neurons},
  author={Jo{\~a}o Paulo Lima Daher and Mingyao Ying and Rebecca Banerjee and Rebecca S. McDonald and Myriam Dumas Hahn and Lichuan Yang and M Flint Beal and Bobby D. Thomas and Valina L Dawson and Ted M Dawson and Darren Moore},
  journal={Molecular Neurodegeneration},
  year={2009},
  volume={4},
  pages={34 - 34}
}
Missense mutations and multiplications of the α-synuclein gene cause autosomal dominant familial Parkinson's disease (PD). α-Synuclein protein is also a major component of Lewy bodies, the hallmark pathological inclusions of PD. Therefore, α-synuclein plays an important role in the pathogenesis of familial and sporadic PD. To model α-synuclein-linked disease in vivo, transgenic mouse models have been developed that express wild-type or mutant human α-synuclein from a variety of neuronal… CONTINUE READING