🧪 A study links pesticide to Parkinson's disease

While cases of neurodegenerative diseases are on the rise, scientists have examined the role of environmental factors. Recent work by UCLA Health provides tangible evidence regarding the impact of a pesticide compound, chlorpyrifos.

The team analyzed information concerning over 1,600 people in California. Their results, published in the journal Molecular Neurodegeneration, indicate that individuals who have lived long-term near areas where pesticides using this compound are sprayed see their likelihood of developing Parkinson's disease increased by a factor of more than 2.5.


To obtain this data, researchers cross-referenced pesticide use registries with the participants' places of residence and work. At the same time, experiments on mice replicated inhalation exposure, comparable to that of humans. Zebrafish were also used to observe cellular mechanisms.

Mice exposed to chlorpyrifos exhibited motor disorders and a loss of dopamine-producing neurons, similar to patients suffering from Parkinson's. Their brains also showed signs of inflammation and protein aggregates. In zebrafish, the pesticide disrupted autophagy, which is a cellular cleaning process.

Although the use of chlorpyrifos is now more or less restricted depending on the country, many people have been exposed to it in the past. Other pesticides with similar properties remain in use.

Dr. Jeff Bronstein, the lead author of the study, points out that this work identifies chlorpyrifos as a specific risk factor, with an identified causal mechanism.

Autophagy, an essential cleaning process for neurons

Autophagy is a cellular mechanism that recycles damaged components. Within neurons, this process is essential for eliminating misfolded proteins and preserving cellular integrity. In the absence of efficient cleaning, this debris accumulates and can lead to cell death.

In the context of neurodegenerative diseases like Parkinson's, autophagy plays a protective role. Its dysfunction is observed in several conditions, which encourages the formation of toxic aggregates. Learning how to stimulate it could help maintain brain functions.

Ongoing work is exploring molecules that could activate autophagy. Such approaches could slow the progression of neurodegeneration. They represent a promising avenue for developing treatments that target the cellular origin rather than just the symptoms.