Rare gene variants may explain why long-term pesticide exposure spikes the risk of developing Parkinson’s disease, a study said on Thursday.
Although pesticide exposure is linked to Parkinson’s disease risk, the new study sought to explain why some individuals with high exposure develop the disease while others do not.
Researchers from the University of California-Los Angeles (UCLA) found that variants in some rare gene variants were enriched in patients with more severe Parkinson’s disease who also had higher exposure to pesticides.
“These variants also appeared to be deleterious to protein function suggesting that disruption of lysosomal activity may be underlying the development of Parkinson’s disease combined with pesticide exposure,” they noted in the paper published in the journal NPJ Parkinson’s Disease.
For the study, the team used genetic data from nearly 800 California residents with Parkinson’s disease, many of whom had long-term exposure to 10 pesticides used on cotton crops for at least a decade before developing the neurological disease.
Their genetic makeup was examined for rare gene variants linked to the function of lysosomes — cellular compartments that break down waste and debris and are thought to be associated with the development of Parkinson’s. It was then compared with high exposure to pesticides.
“While the specific interactions between pesticides and the expression of these genetic variants require further study, the results suggest that in someone with such variants, long-term exposure to the cotton pesticides could lead to the buildup of toxic compounds, due to alterations of the cells’ ability to break down damaged proteins and organelles — a process known as autophagy — and thus lead to Parkinson’s disease,” Dr Brent Fogel, corresponding author and professor of Neurology and Human Genetics at UCLA, said.
“On a day-to-day basis, these variants are not having much of an impact. But under the right stress, such as exposure to certain pesticides, they can fail and that could, over time, lead to the development of Parkinson’s disease. This is called a gene-environment interaction,” Fogel said.
