Parkinson’s disease (PD) has been classically considered a predominantly
environmentally related disorder with known etiologies, including MPTP
toxin exposure, carbon monoxide exposure, postencephalitic related (1919
epidemic), manganese exposure, and other putative chemical exposures
involving injury to mitochondrial complex I enzymes. Nevertheless, most
cases are idiopathic without demonstrable etiology, and clearly some cases
are genetically influenced. The knowledge that PD is related to progressive
dopaminergic cell loss in the substantia nigra with symptomatology usually
appearing at 80 to 90% cell depletion and the evidence connecting Parkinsonism
to environmental exposures has led to an oxidative stress theory for
the pathogenesis of PD and an emphasis on apoptosis as a possible mechanism
of cell loss.