Impact of Environmental Risk Factors on Mitochondrial Dysfunction, Neuroinflammation, Protein Misfolding, and Oxidative Stress in the Etiopathogenesis of Parkinson's Disease.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and epidemiological literature without systematic search methodology
PubMed 36142718 · doi:10.3390/ijms231810808
What was done
This narrative review synthesizes cellular, animal, and human epidemiological evidence on environmental risk factors in sporadic Parkinson's disease. It evaluates mechanistic pathways—including mitochondrial dysfunction, neuroinflammation, protein misfolding, and oxidative stress—associated with exposures to pesticides and herbicides (MPTP, rotenone, paraquat, DDT, dieldrin), heavy metals (manganese, vanadium), traumatic brain injury, industrial chemicals, farming, well-water consumption, and rural living.
What was found
The abstract reports no numerical data, risk estimates, or quantitative findings. It describes qualitative positive associations between Parkinson's disease and exposure to specific neurotoxic chemicals and environmental factors, outlining their shared contributions to nigrostriatal dopaminergic neurodegeneration and Lewy body pathology.
Why it matters
It organizes diverse toxicological exposures under unified mechanistic pathways, helping contextualize how environmental neurotoxicants might initiate or accelerate dopaminergic loss in sporadic Parkinson's disease.
Limits
The abstract provides no quantitative metrics, effect sizes, or counts of reviewed studies. As a narrative review, it does not employ systematic search methods, risk of bias assessment, or meta-analysis, and relies heavily on preclinical models that may not reflect real-world human exposure levels.
Cited by
- supports Exposure to organic toxicants such as trichloroethylene (TCE), perchloroethylene (PCE), dieldrin, and paraquat contributes to the risk and pathology of Parkinson's disease.