Los Angeles, California 90095


Purpose:

Parkinson's disease (PD) occurrence is higher in rural than in urban populations of industrialized countries. Epidemiologic and human tissue studies suggest that pesticides may be responsible for causing dopaminergic cell death at increased rates. While many pathophysiologic pathways may be involved in the neurodegeneration responsible for PD, genetic factors are likely to determine a general susceptibility to neurodegeneration.


Study summary:

While many pathophysiologic pathways may be involved in the neurodegeneration responsible for PD, genetic factors are likely to determine a general susceptibility to neurodegeneration. There are a number of genetic polymorphisms of genes such as those coding for the cytochrome p450 super-family of genes referred to as 'susceptibility genes'. However, they are generally not sufficient to cause disease unless a person encounters exposure to an environmental toxin: the disease is caused by a gene-environment interaction. Thus, it is imperative to assess genetic susceptibility in individuals exposed to a toxin. We will test the gene-environment interaction hypothesis by conducting an epidemiologic population-based case-control study of newly diagnosed PD patients from three rural California counties: Kern, Fresno, and Tulare. Over a four year period, we expect to collect 400 cases referred to us by local neurologists, farm worker clinics, and Parkinson's foundations. For each case, one population control will be selected at random from residential parcel maps and Medicare databases and, in addition, one unaffected sibling control and - when possible - affected siblings to avoid potential biases and inefficiencies inherent in the use of each type of control. For each study subject, an environmental and occupational pesticide exposure estimate will be derived using California pesticide-use reporting (PUR) data and information about pesticide application on crops in combination with crop patterns shown in satellite images and aerial photographs; in addition, extensive exposure interviews will be conducted with all study subjects. In a three-tiered approach to examine the effects of gene-environment interactions we will: 1) test for association (and linkage) of PD to selected loci associated with PD in earlier studies using multiallelic repeat markers and genotyping; 2) test for association using intragenic single nucleotide polymorphisms (SNPs) of 50 candidate genes arrayed to create "the PD array"; and 3) use future technical possibilities to screen for genome wide associations using array technology to scan 5,000-10,000 SNPs throughout the genome. Data analysis will employ hierarchical modeling procedures to take into account multiple comparison issues and to incorporate prior knowledge such as increased neurotoxicity due to the interaction of gene products and chemicals.


Criteria:

Newly diagnosed patients with idiopathic PD (first PD diagnosis after January 1998 who are currently living in one of the three target counties (Kern, Tulare, Fresno) and have lived in California for at least 5 years are eligible for participation. For each patient, one or more unaffected sibling controls and one population control will be recruited. The population control are being selected randomly from Medicare records (95% of all controls) and residential parcel listings (for those patients younger than 65 years of age only; the same inclusion criteria will be applied as to the cases. The controls are being marginally matched to cases according to 5-year age categories (e.g. 50-54, 55-59, 60-64, etc.), race (white, African-American, Asian, Hispanic, other), and sex. All study cases by definition will be patients who elicited care from health care providers. We are aiming to enroll every newly diagnosed PD patient into our study and expect patient population participating in our study that is as diverse as the rural population.


NCT ID:

NCT00044590


Primary Contact:

N/A


Backup Contact:

N/A


Location Contact:

Los Angeles, California 90095
United States

Beate R Ritz, MD, Ph.D.
Phone: 310-206-7458
Email: britz@ucla.edu

Site Status: Recruiting


Data Source: ClinicalTrials.gov

Date Processed: December 17, 2017

Modifications to this listing: Only selected fields are shown, please use the link below to view all information about this clinical trial.


Click to view Full Listing

If you would like to be contacted by the clinical trial representative please fill out the form below.