How air pollution may contribute to the onset of Parkinson’s disease
At the University of California Los Angeles, a coalition of researchers were able to demonstrate how the chemicals found in diesel exhaust may lead to alpha-synuclein build-up, contributing to the possible onset of Parkinson’s disease.
As published in Toxicological Sciences, the UCLA-based group focused on identifying environmental factors as opposed to genetic risks for the development of neurodegenerative diseases in older adults.
“Epidemiological studies have supported an association between long-term exposure to air pollutants and disease risk,” the co-authors explained in their findings. “Here, we investigate the mechanisms by which diesel exhaust, a major component of air pollution, induces neurotoxicity.”
In past research studies, it was suggested that people living near areas with a high volume of traffic-related air pollution were more likely to be diagnosed with Parkinson’s disease.
In the new study, UCLA researchers set out to understand the effects of air pollutants by using a zebrafish model and testing with diesel exhaust.
According to the findings, it was concluded that exposure to diesel exhaust perpetuated effects implicated in neurodegeneration.
“We found that exposure to diesel exhaust particulate extract caused behavioral deficits and a significant decrease in neuron number,” the findings read. “The neurotoxicity was due, at least in part, to reduced autophagic flux, which is a major pathway implicated in neurodegeneration. This neuron loss occurred alongside an increase in aggregation-prone neuronal protein.”
Using nilotinib, a selective tyrosine kinase receptor inhibitor, the diesel exhaust-induced neurotoxicity was inhibited among the zebrafish examined in the lab.
“These results shed light on why long-term exposure to traffic-related air pollution increases neurodegenerative disease risk and open up new avenues for exploring therapies to mitigate environmental exposures and promote neuroprotection,” the co-authors concluded.