Our faculty, Drs. Beate Ritz, Jeff Bronstein, and Yvette Bordelon from Epidemiology and Neurology at the UCLA Fielding School of Public Health and Geffen School of Medicine have been studying Parkinson’s disease among residents of Kern, Fresno, and Tulare counties with funding from the National Institute of Health since 2001. We were able to address important questions concerning the causes of Parkinson’s disease (PD) with the information we gathered for more than 2,000 individuals. We are also continuing to follow-up participants to gain a better understanding of progression in Parkinson’s disease (PD) with the hope to learn how to slow disease down or eventually stop progression.
We have and continue to learn about the causes and progression of Parkinson’s disease due to the great effort and kindness of people with and without PD who participate in our study along with those who care for them. We are grateful and humbled by your continuing support of this effort. Thank you!
New insights we have gained thus far:
Pesticides are Linked to Parkinson’s Disease. We have continually built a case that a number of specific pesticides contribute to Parkinson's disease onset. To date, we have tied the following pesticides to increases in PD risk: paraquat, maneb, ziram, benomyl (banned in 2000), and a large number of organophosphate pesticides including diazinon and chlorpyrifos. It is important to recognize that some people are more vulnerable to the harmful action of pesticides due to age or genetics. Pesticides use biologic mechanisms such as impairing mitochondrial function to increase PD risk, especially in individuals whose systems cannot defend them well enough against pesticide toxicants due to their genetic make-up. We have also shown that pesticides, including organophosphates, contribute to faster disease progression.
Household Pesticide Use and Parkinson's Disease. We found that frequent use (once a month or more) of any household pesticide in and around homes, gardens and yards increases the odds of developing PD, especially products containing organophosphorus chemicals. Our results did not change when we took other pesticide exposures (ambient and occupational exposures) into account.
Head Injury and Paraquat Exposure and the Alpha-synuclein Gene. Head injuries are especially bad for those exposed to pesticides/herbicides such as paraquat and those who in addition carry a genetic risk factor in the alpha-synuclein gene. Those participants with head injuries who lived or worked near areas where paraquat had been applied were several times more likely to develop PD.
Development of Depression in Parkinson's Disease. Major life events (death of a spouse or close friend or family member; separation or divorce; being laid off or fired from work; sudden illness or injury in someone close; loss of home; retirement; experience of assault or robbery; involvement in serious accident) play an important role for onset of depression in patients with PD. Patients who receive more support from family and neighbors are, however, less affected and positive social interactions seems to protect against depression in PD.
Genetic Factors and Cognition in Parkinson's Disease. Cognitive impairments, including dementia, are unfortunately common when disease progresses. We identified a remarkably wide range of cognitive impairments in PD patients. In collaboration with the University of Washington, Seattle, we identified genetic factors affecting cognition in PD including the APOE ε4 gene, known for its role as a risk factor for Alzheimer disease.
Chemical Marker of Rapid Motor Progression. We found a chemical signature in blood that predicts rapid motor progression. We also identified markers that suggest the immune system of PD patients ages faster. This is an important step forward in understanding how Parkinson's disease evolves over time.
Parkinson’s Disease Linked to Immune System Aging: Aging has long been related to PD and it has been proposed that PD patients may exhibit signs of faster aging. For the first time, using DNA based markers of aging in the blood, known as the “epigenetic clock,” we found that the immune system of PD patients was aging faster than that of non-patients. We also found differences in blood cell counts between PD patients and non-patients, demonstrating a larger role for the involvement of the immune system in PD.
Vitamin D and Cognition in Parkinson’s Disease: It has been suggested that Vitamin D influences susceptibility for Parkinson’s disease (PD), Alzheimer’s disease or overall cognition functioning in the elderly. We found that for PD patients followed for an average of 7.1 years into disease, Vitamin D receptor genetics linked to Vitamin D function were important for cognitive decline. This suggests that Vitamin D might play a role in cognitive decline in PD. However, additional studies are needed to clarify its role further.