Although an increased immunoreactivity for effectors of the mitochondrial apoptotic pathway (e.g. caspase 3) (Tatton 2000), an increased activation of JNK downstream targets (Hunot et al. 2004), as well as nuclear accumulation of GAPDH (Tatton 2000) have been detected in post-mortem SN of PD patients, there is still no clear consensus concerning the contribution of apoptosis to loss of DAergic neurons in PD (Tatton et al. 2003b). This evidence concerns the gene CASP3 and Parkinson disease.