The Relationship Between Pesticide Exposure and Neurodegenerative Diseases: A Mini-Review

Context: Pesticides are widely used in agriculture and household settings and have been associated with various adverse health effects, including a potential link to neurodegenerative diseases (NDs). Alzheimer s disease (AD) and Parkinson s disease (PD) are the two most common disorders in this category, characterized by progressive neuronal cell loss and severe impairments in human functioning. Epidemiological studies have shown significant associations between pesticide exposure—specifically organochlorines, organophosphates (OP), carbamates, DDT, and paraquat—and AD and PD; however, little is known about the underlying biological mechanisms. Evidence Acquisition: A mini-review was conducted in the scientific literature on the biological mechanisms linking pesticide exposure to NDs using scientific databases (PubMed, Scopus, Web of Science, and Google Scholar). Results: In AD, the connection may involve several biological mechanisms, including hyperphosphorylation of tau protein, which disrupts normal cellular function and contributes to neurofibrillary tangles. Genetic polymorphisms in microtubule-associated protein tau (MAPT) can also influence an individual s susceptibility to AD by affecting tau protein interactions with microtubules. Moreover, exposure to pesticides has been linked to elevated pro-inflammatory markers that exacerbate neuroinflammation, further contributing to neuronal damage. In PD, oxidative stress plays a crucial role by generating reactive oxygen species that damage cellular components. Mitochondrial dysfunction resulting from pesticide exposure impairs energy production in neurons, leading to cell death. Additionally, exacerbation of α-synuclein aggregation is a critical factor in PD pathology, as aggregated forms of this protein are toxic to neurons. Conclusions: Given the rapid increase of pesticides in the air, water, and food, it is essential to clarify the biological mechanisms linking pesticide exposure to NDs.