“…Thus, although defects in mitochondrial ETS may be present in some patients with PD, the absence of such defects in these 12 patients with early PD indicates that they cannot be essential to the pathogenesis of neuronal death in early PD. (Kuhl et al, 1984;Leenders et al, 1985;Eidelberg et al, 1993Eidelberg et al, , 1994Piert et al, 1996). In one of these studies, reductions in global CMRglc were seen only after L-DOPA was administered, suggesting that the reduction in metabolism may be at least, in part, because of medication effects (Piert et al, 1996).…”