Assessing the Impact of Environmental Chemicals on the Development of Neurodegenerative Diseases Across Biological Systems

Abstract

Introduction: Neurodegenerative diseases, especially Alzheimer’s Disease (AD) and Parkinson’s Disease (PD) are a complex health problem with a significant prevalence across the world that is fueled by multifactorial etiology. Although genetic factors are important, the evidence points towards environmental toxicants as important, alterable risk factors to the onset and progression of these diseases. Neurodegeneration in later life is also increasingly associated with exposure to industrial and environmental toxins, which usually happen pre- and post-natally. Materials and Methods: The abstract is a synthesis of the findings of two general literature reviews, which assessed epidemiological and experimental studies of the effects of environmental pollutants on AD and PD. The analyzed literature has been united on the issue of chemical classes and neurotoxicity with the help of the different in vivo models (e.g., rats and mice) and in vitro models (e.g., SH-SY5Y cell lines) to determine the causal relationships and molecular mechanisms. Animal studies also demonstrate that chronic exposure to environmental toxicants disrupts neuronal function in wildlife and laboratory species, producing pathological changes similar to those seen in AD and PD. These cross-species neurotoxic responses highlight the broader ecological burden of chemical contamination and its relevance to human neurodegenerative risk.

Results and Discussion: It was consistently found that a wide range of environmental pollutants are implicated in the development of both illnesses, including heavy metals (such as lead, aluminum, mercury, arsenic, cadmium, and manganese), pesticides (such as organophosphates and paraquat), industrial solvents like trichloroethylene (TCE), and various air pollutants. The underlying etiology is commonly associated with increased oxidative stress and mitochondrial dysfunction. Specifically, these neurotoxic agents promote key pathological features of Alzheimer’s disease, including the elevation of Aβ peptide levels and the hyperphosphorylation of Tau protein, which together contribute to the formation of amyloid plaques and neurofibrillary tangles (NFTs). In Parkinson’s disease, exposure to these toxicants is linked to the aggregation of alpha-synuclein (α-syn), resulting in the formation of Lewy bodies (LBs) and leading to progressive nigrostriatal dopaminergic degeneration. Another major mechanism involves the reduced activity of Aβ-degrading enzymes and various epigenetic modifications that further exacerbate neurodegenerative processes.

Conclusion: The synthesis of epidemiological and experimental data indicates the high risk of the environment on the health of a significant group of people. This creates a pressing necessity of preventive measures to reduce contamination and requires additional studies aimed at determining certain biomarkers and creating in vivo models to detect the early signs of neurodegeneration and establish specific, effective interventions to prevent contamination by pollutants.