UCLA Health announced on May 19 it will lead a $9 million, multi-institutional research project to investigate how exposure to pesticides and air pollution may influence the risk and progression of Parkinson’s disease.
The study aims to clarify the genetic and environmental factors that determine why some individuals develop Parkinson’s disease more quickly than others. Researchers hope their findings could eventually contribute to new treatments or prevention strategies for this neurodegenerative disorder.
The three-year project is funded by Aligning Science Across Parkinson’s in partnership with The Michael J. Fox Foundation for Parkinson’s Research, as part of an expansion of ASAP’s Collaborative Research Network. UCLA will collaborate with Cedars-Sinai and the University of Münster in Germany, analyzing populations exposed to pesticides and air pollution, stem cells derived from affected individuals, as well as animal models. Project lead Dr. Jeff Bronstein said, “We have known for some time about the risks of chronic exposure to these commonly used pesticides and air pollution, but the mechanisms underlying these risks still remain unclear. We seek to deepen our understanding of the specific pathways impacted by exposure to these toxicants, which we hope can lead to treatments to prevent more cases of Parkinson’s disease or slow disease progression.”
Previous studies led by Dr. Beate Ritz at UCLA found higher risks among Central Valley residents exposed over time to certain pesticides such as chlorpyrifos and paraquat or small particulate matter in air pollution. The current hypothesis is that both environmental exposures and genetics play a role in accelerating disease onset.
The new research will use advanced genetic and protein analyses on human brain cells made from stem cells collected from people with varying levels of pollutant exposure in California’s Central Valley. Animal models like zebrafish and mice will also be studied alongside human cells; researchers plan genetic modifications aiming at slowing or halting disease development.
Parkinson’s disease results from damage or death of nerve cells responsible for producing dopamine—a chemical essential for muscle movement—causing symptoms such as tremors, slowed movement, freezing gait, or stiff muscles. About one million people live with Parkinson’s in the U.S., while worldwide cases reach ten million; diagnoses have nearly doubled nationally over the past decade according to the official website.
Drs. Beate Ritz, Chao Peng, William Zeiger, Jesus Araujo and Kimberly Paul (all UCLA), along with Dr. Christina Lill (University of Münster), are co-principal investigators on this effort set to begin in June through 2029.
A separate ASAP- and Michael J. Fox Foundation-supported collaboration between UCLA researchers—including Rosalie Lawrence—and University of Dundee scientists will explore how cellular stress pathways interact with mitochondrial function related to Parkinson’s risk: “We seek to understand how these pathways crosstalk and compensate in the context of Parkinson’s disease progression by studying mitochondrial clearance in situ in cultured dopaminergic neurons and human brain samples, paving the way for the development of new therapeutic strategies that restore mitochondrial function,” Lawrence said.
The University of California Los Angeles operates within the University of California system; it has gained national acclaim through achievements including Nobel laureates while fostering diverse perspectives across its 419-acre campus supporting academic excellence according to its official website.
