Scientists to study link between pesticides and Parkinson’s

Scientists at Cedars-Sinai Health Sciences University are part of a team that will use a $9 million grant from the Aligning Science Across Parkinson’s (ASAP) initiative to study the connection between exposure to pesticides and air pollutants and the risk of developing Parkinson’s disease.

The grant is part of ASAP’s Collaborative Research Network (CRN), a global community of multidisciplinary and multi-institutional teams working to understand disease variability. The network is managed by the Coalition for Aligning Science and implemented by The Michael J. Fox Foundation (MJFF).

“With this grant, we will generate lines of stem cells from people living in a pesticide-treated area in the San Fernando Valley and attempt to figure out why some developed Parkinson’s and some did not,” said Clive Svendsen, PhD, executive director of the Cedars-Sinai Board of Governors Regenerative Medicine Institute, said in a university news story. “We are trying to determine which … genetic vulnerabilities interact with pesticides—and how. If we can figure that out, we can begin to think about new approaches to treatment.”

The study is part of a project, “Environmental & Genetic Determinants of Parkinson’s Disease Progression,” which includes researchers from two U.S. universities — University of California Los Angeles and the University of Southern California – and the University of Münster in Germany.

Parkinson’s disease is caused by the progressive loss of dopaminergic neurons, the nerve cells responsible for making dopamine. Dopamine is a molecule that nerve cells use to communicate, involved in motor control. Most people with Parkinson’s have no specific disease-related gene or a single genetic cause, while about 5% to 10% of cases are caused by mutations in a single gene. Evidence suggests that mutations in a set of genes may increase the risk of developing Parkinson’s.

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‘Genes load the gun, while the environment pulls the trigger’

“We think that Parkinson’s disease is caused by a combination of genetic traits in the patient and environmental exposures—especially to certain pesticides and air pollution,” said Svendsen, who is a principal investigator on the project. “It seems the genes load the gun while the environment pulls the trigger.”

The researchers will recruit groups of relatives in which some developed Parkinson’s and others did not. They will use induced pluripotent stem cells (iPSCs) derived from participants’ cells, reprogrammed into a stem-cell-like state, and differentiated into dopaminergic neurons. These cells will then be exposed to pesticides or air pollutants present in the areas where the participants live.

The team focuses on two specific pesticides — copper sulfate, a compound used to eliminate fungi, bacteria, and algae — and 2,4-dichlorophenoxyacetic acid, an herbicide used to kill broadleaf weeds.

Researchers hypothesize that dopaminergic neurons derived from people with Parkinson’s will die more quickly after exposure to pesticides or air pollutants than neurons from family members exposed to the same agents who did not develop the disease. They can then compare participants’ genetic and protein profiles to understand what triggers Parkinson’s development in some individuals but not in others.

“By investigating how the environment and a person’s unique genetics interact to drive Parkinson’s, this team is uncovering the diverse biological drivers of the disease,” said Sonya Dumanis, PhD, managing director of ASAP. “With a better understanding of these disease mechanisms, we can lay the groundwork for new, personalized therapeutics and better outcomes for Parkinson’s patients.”