LOW PLATELET MITOCHONDRIAL COMPLEX-I AND COMPLEX-II III ACTIVITY IN EARLY UNTREATED PARKINSONS-DISEASE/

Following the discovery of inhibition of electron transport complex I by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which produces a parkinsonian syndrome in humans, monkeys, and mice, several laboratories have reported abnormalities of complex I and othe r electron transport complexes (ETCs) in various tissues from patients with Parkinson's disease (PD). Criticism of the significance of these findings in the etiology of PD has centered on whether drug- treatmen ts or the debilitation of the disease process itself produced the low ETC activities. We present results from a blinded study of platelet mi tochondrial ETC activities in 18 early untreated PD patients and 18 ag e- and sex-matched controls and in 13 spousal controls. Lower complex I activity in platelet mitochondria of PD patients was seen in early u ntreated disease and thus cannot be due to debilitation or drug therap y. Home environmental factors seem an unlikely explanation for the red uced complex I activity in PD patients but have not been excluded. Com plex II/III activity was also reduced by 20% in PD compared with age-/ sex-matched controls. The low complex I and II/III activities in plate let mitochondria appear to be related to the etiology of PD.