The scientific community has long debated the origin of the toxic proteins that cause Parkinson’s disease, with some researchers suggesting that the disease begins outside the brain. A new hypothesis paper, published in the Journal of Parkinson’s Disease on World Parkinson’s Day, suggests that the disease may result from processes that start in either the brain’s smell center or the body’s intestinal tract. The authors of the study argue that environmental toxicants, such as certain pesticides, dry cleaning chemicals, and air pollution, may play a role in the development of Parkinson’s disease.
The misfolded protein alpha-synuclein, which accumulates in the brain in clumps known as Lewy bodies, has been identified as a key factor in Parkinson’s disease. The new study proposes that exposure to environmental toxins, such as the chemicals trichloroethylene and perchloroethylene, the herbicide paraquat, and air pollution, may contribute to the formation of toxic alpha-synuclein. These toxins are found in various industrial and commercial sites, as well as in widely used herbicides in the US. Air pollution has also been linked to the disease, with high levels of pollution noted in nineteenth century London where Parkinson’s was first described.
The nose and gut have close connections to the brain and are lined with permeable tissue, making them potential entry points for environmental toxins. In the brain-first model, chemicals are inhaled and may enter the brain through the nerve responsible for smell. From there, alpha-synuclein spreads to other parts of the brain, particularly regions with dopamine-producing neurons, leading to cell death that characterizes Parkinson’s disease. Conversely, ingestion of toxins through the gastrointestinal tract may result in alpha-synuclein pathology in the gut’s nervous system, which then spreads to both sides of the brain and spinal cord.
The timing, dose, and duration of exposure to environmental toxins, as well as interactions with genetic and other factors, may determine who ultimately develops Parkinson’s disease. The authors of the study believe that their hypothesis may help connect specific exposures to specific forms of the disease, and increase public awareness of the adverse health effects of environmental chemicals. This new understanding of the role of environmental toxicants may also shed light on how they contribute to other brain disorders, such as autism, ALS, and Alzheimer’s disease.
The authors of the hypothesis paper, including experts from the University of Rochester and other institutions, suggest that their models of environmental exposure could advance understanding of various brain diseases. They are organizing a symposium in Washington, DC, to explore the role of toxicants in food, water, and air in these diseases. By linking environmental exposure to brain disorders, researchers hope to ultimately prevent these diseases and improve public health outcomes.
