New Research Suggests That Environmental Toxins, Whether Inhaled Or Ingested, Might Trigger Parkinson’s Disease And Result In Various Distinct Subtypes
Approximately 1 million people in the United States are living with Parkinson’s disease, and this figure is projected to rise to 1.2 million by 2030, according to the Parkinson’s Foundation.
This brain disorder leads to involuntary movements and tremors. Over time, it can also progressively impair abilities like walking and talking.
Each year, about 90,000 Americans are diagnosed with Parkinson’s, so as the number of cases increases, experts are investigating the causes behind the disorder.
Now, a new study conducted by researchers at the University of Rochester suggests that environmental toxins, whether inhaled or ingested, might trigger the disease, potentially resulting in various distinct subtypes of Parkinson’s.
This theory expands on the “brain-first vs body-first” model of Parkinson’s. According to this model, the onset of the disease can occur in one of two primary locations: the brain, specifically starting from the olfactory bulb, which is responsible for smell, or the body, beginning within the gut’s nervous system.
“In both the brain-first and body-first scenarios, the pathology arises in structures in the body closely connected to the outside world,” explained Dr. Ray Dorsey, the study’s co-author.
“Here we propose that Parkinson’s is a systemic disease and that its initial roots likely begin in the nose and in the gut and are tied to environmental factors increasingly recognized as major contributors, if not causes, of the disease,” Dr. Dorsey continued.
“This further reinforces the idea that Parkinson’s, the world’s fastest-growing brain disease, may be fueled by toxicants and is therefore largely preventable.”
From these initial locations, the progression of the disease is characterized by accumulations of a protein known as alpha-synuclein, which spreads in a predictable pattern.
Sean A E/peopleimages.com – stock.adobe.com – illustrative purposes only, not the actual person
Cases that begin in the brain typically exhibit early motor difficulties, with problems such as constipation arising later. Conversely, cases that start in the body often show early symptoms like sleep disturbances and a more uniform onset of motor symptoms.
As for what triggers the initial misfolding and aggregation of the protein alpha-synuclein, the research team suggests that, in cases of brain-first Parkinson’s, inhaled toxicants might be responsible.
For instance, agricultural pesticides such as paraquat, which have a strong association with the disease, may enter the brain via the nasal route.
Similarly, toxic solvents like trichloroethylene (TCE) and perchloroethylene (PCE), which are commonly used in dry cleaning, can vaporize into the air and be inhaled. Additionally, even air pollution, particularly fine particulate matter, has been linked to an increased risk of Parkinson’s.
Conversely, for body-first Parkinson’s, the researchers suggest that ingested toxicants may initiate the clumping of alpha-synuclein in the gut. Pesticides, for example, can infiltrate well water and the broader food supply, with consumption of such water being associated with Parkinson’s.
Certain pesticides specifically have been linked to body-first symptoms like REM sleep behavior disorder. Additionally, industrial chemicals like TCE can contaminate groundwater.
One study even showed that Marines at Camp Lejeune, who drank water contaminated with TCE for more than three decades, faced a 70% increased risk of developing Parkinson’s.
“These environmental toxicants are widespread, and not everyone has Parkinson’s disease. The timing, dose, and duration of exposure and interactions with genetic and other environmental factors are probably key to determining who ultimately develops Parkinson’s,” said Dr. Dorsey.
“In most instances, these exposures likely occurred years or decades before symptoms develop.”
This theory also leads to hypotheses that can be tested moving forward. The research team speculates that the prevalence of Parkinson’s will align with levels of toxicant exposure across different regions.
Inhaled toxicants may correlate with brain-first cases, while ingested toxicants with body-first cases.
So, as certain countries reduce the use of harmful chemicals, the incidence of Parkinson’s might decrease. On the flip side, in industrializing countries where pollution is increasing, rates might climb.
Distinct brain imaging patterns could emerge in affected individuals, depending on whether the toxicants were inhaled or ingested.
Furthermore, in animal models, exposure to inhaled toxicants is expected to induce a brain-first pattern of alpha-synuclein pathology, whereas ingested toxicants should lead to a body-first pattern.
To read the study’s complete findings, which have since been published in the Journal of Parkinson’s Disease, visit the link here.
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