A53T a-synuclein

Giasson, B.I. et al. Neuronal a-synucleinopathy with severe movement disorder in mice expressing A53T human a-synuclein. Neuron 34 521-533, 2002. 

A mouse spontaneous deletion strain is viable, fertile, and phenotypically normal (Specht and Schoepfer, 2001) whereas overexpression of wild-type SNCA in a mouse model has many features of PD, such as loss of dopaminergic terminals in the striatum, mislocalization and accumulation of insoluble a-synuclein, and motor abnormalities (Rockenstein et al., 2002 Fleming et al., 2004 Masliah et al., 2000). Both A30P and A53T mutant mouse models display neuronal cell loss and motor changes (Melrose et al., 2006). 

Ono K, Ikemoto M, Kawarabayashi T et al. (2009) A chemical chaperone, sodium 4-phenylbutyric acid, attenuates the pathogenic potency in human alpha-synuclein A30P -E A53T transgenic mice. Parkinsonism Relat Disord 15, 649-654. 

Kohl Z, Winner B, Ubhi K et al (2012) Fluoxetine rescues impaired hippocampal neu-rogenesis in a transgenic A53T synuclein mouse model. Eur J Neurosci 35 10-19... 

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