The etiology of PD seems to be multifactorial, with genetics, aging, environmental agents all playing etiological roles. However, the molecular and neural mechanisms responsible for the age-enhanced disease vulnerability remain unknown. A loss of a dopaminergic phenotype is consistently seen in normal aging (Beal, 1992; Levy et al., 2005; Biskup and Moore, 2006; Chu and Kordower, 2007). This is especially notable since striatal dopamine insufficiency is the key pathological feature responsible for most of the cardinal signs seen in PD. However, it is clear that aging is just a component of PD pathogenesis and other factors, for example genetics or exposure to toxic events, may be superimposed upon age-related losses in striatal dopamine and these, in combination, drive striatal dopamine insufficiency to a level that causes symptoms (Di Monte et al., 2002; Jellinger, 2004; Chu and Kordower, 2007). We know that the main action of antipsychotic drugs is to reduce dopamine level in some brain areas including the substantia nigra. So could this mechanism in the long run induce PD?