In this study of monozygous and heterozygous twins, researchers found that genetic susceptibility played a role in early-onset PD where symptoms are seen prior to age 50. In the vast majority of cases, though, where PD develops after age 50, genetics was not the determining factor. Presumably some other factor, possibly of environmental origin, accounts for the majority of PD in this country. Important insights into environmental triggers of PD were gained in the early 1980s when a synthetic heroin elicited severe Parkinsonism in addicts who injected it intravenously. Subsequent case-control studies have found increased incidence of PD associated with pesticide use, rural environments, consumption of well water, exposure to herbicides, and living near industrial plants, printing plants, or quarries.
Additional research is directed toward defining the biochemical pathways of early PD development.
Findings from such work could potentially lead to therapeutic interventions. Mixtures of lead, copper and iron posed a greater risk than exposure to any of these metals singly. This work is examining whether these agents, acting in concert with normal nervous system aging, increase PD risk. To do this research, some of the neurons in normal mouse midbrain tissue will be genetically altered, creating a mosaic of normal and altered cells which will then be exposed to a relevant toxic agent to see whether the altered cells are selectively affected relative to normal neurons. Since PD is a malfunctioning of the dopaminergic systems of the brain, this work could have important implications in PD, as well as other neurodegenerative diseases, that operate through this mechanism.