(conducted at the Division of Research in conjunction with Stanford University and The Parkinsons Institute; Funded by: NINDS)
The Parkinsonism Epidemiology at Kaiser or PEAK study sought to evaluate the contribution of environmental and genetic risk factors to the etiology of Parkinson's disease (PD). Of particular interest are substances that are similar in chemical structure or mechanism of action to established toxicants for secondary parkinsonism, a disorder that shares some clinical and pathological features with idiopathic PD. The focus was on settings where high dose or chronic exposure may have taken place, specifically, the agricultural impaired toxicant metabolism, the CYP2D6 gene that encodes for the P450 enzyme debrisoquine hydeoylase, was measured. This is a common enzymatic pathway for the metabolism of many of the neurotoxicants under study. The role of putative protective factors (i.e. dietary antioxidants, cigarette smoking, skin pigmentation) that may minimize the toxicity of exogenous exposures were also evaluated. We have completed a case-control study of 496 incident PD cases identified within the KPMCP of Northern California. Rigorous CAPIT/Hughes diagnostic criteria were applied by a movement disorder specialist. Control subjects (n=541) were selected from computerized KPMCP membership files and matched to cases by gender and age. Study information was collected by structured interview and included: demographic characteristics, residence history, lifetime occupational history, hobbies, home exposures, illicit and prescription drug use, family history, cigarette smoking and dietary habits. Blood samples were drawn for genetic studies. It is hoped that the study will advance knowledge of potential neurotoxic and genetic risk factors for PD in a racially and geographically diverse population.