Lately, a notable growth of Parkinson’s disease has been observed. Between 1990 and 2015, the number of people affected doubled to exceed 6 million. Projections suggest this total could rise to more than 12 million by 2040, underscoring the urgency of understanding its causes and prevention.
The progressive loss of brain neurons is tied to misfolding and aggregation of the alpha-synuclein protein. These toxic aggregates damage dopaminergic neurons in the substantia nigra, a brain region crucial for producing dopamine. The decline of these cells underpins the characteristic symptoms of Parkinson’s disease.
danger in the environment
Family history accounts for about 15% of cases, often linked to inherited variants and undiscovered genetic changes in genes such as LRRK2, PARK7, PINK1, PRKN, or SNCA.
However, most cases appear to be triggered by environmental factors and modifiable risks. Repeated head impacts from activities like football and exposure to pesticides and other chemicals stand out as key influences. The focus here is on pesticide exposure and its possible connection to Parkinson’s disease.
Evidence shows that farmers may be more susceptible to Parkinson’s than the general population. It is important to note that while many people are routinely exposed to pesticides, those who are genetically predisposed may face a higher risk of developing the disease.
On the trail of the microbiota
Pesticide use affects not only crops but also animals and people. Researchers have identified ten products, including insecticides, fungicides, and herbicides, that can adversely influence neurons. These substances may contribute to mechanisms linked to Parkinson’s disease.
How do these neurotoxic effects arise? The presence of these products can disrupt the gut microbiota and shift metabolic processes, leading to the accumulation of problematic metabolites and a modified form of alpha-synuclein in the intestines. Misfolded alpha-synuclein can travel from enteroendocrine cells, which regulate digestion and metabolism, to the brain via the vagus nerve. In the brain, these misfolded proteins can form Lewy bodies, deposits associated with Parkinson’s disease.
List of charges against pesticides
The article explains how certain pesticides and, in light of recent research, some herbicides may be toxic to neurons.
- Glyphosate, the most widely used herbicide worldwide, can disrupt the balance of gut bacteria and promote growth of bacteria that produce brain-damaging metabolites. Animal studies have shown that glyphosate can alter brain neurotransmitters, trigger inflammatory responses, disturb cellular energy, and induce oxidative stress. Exposure is also linked to higher levels of a urinary biomarker of neuronal damage.
- Rotenone, a classic pesticide, is associated with alpha-synuclein accumulation in the brain. Brief exposure can mimic Parkinsonian symptoms, which may worsen over time. Experimental work in mice showed increased harmful alpha-synuclein in digestive and brain pathways, degeneration of dopaminergic neurons, and motor impairment. Microbial analyses revealed shifts in gut bacteria; later studies confirmed motor and neural changes after exposure.
- Deltamethrin, another pesticide, can disrupt dopamine signaling. In mouse studies, exposure led to changes in dopamine pathways, reduced motor function, and cognitive effects, suggesting that adult intake may influence gut-brain development relevant to Parkinson’s.
- Benomyl, a fungicide, has been linked to an increased disease risk by inhibiting aldehyde dehydrogenase, an enzyme essential for metabolizing fats, proteins, and toxins such as alcohol. Inhibition can have detrimental effects on brain health.
Controversial regulation
Understanding the mechanisms of pesticide and herbicide toxicity is crucial for developing preventive strategies and treatments. While some regulatory bodies have allowed broader use of certain chemicals, emerging research supports concerns about neurological and carcinogenic risks.
It is possible that commercial interests influence policy decisions. While intrinsic factors like age, gender, and genetics cannot be changed, environmental factors are within reach. The trajectory of risk may shift with new regulations and safety practices aimed at reducing exposure and protecting public health.
Acknowledgment of ongoing research highlights the need for vigilant assessment and policy updates to safeguard communities and ecosystems.