Researchers found that patients with Parkinson's disease have increased brain levels of iron, especially in the substantia nigra, and decreased levels of feritin, which serves as a protective mechanism by chelating, or forming a ring around the iron, and isolating it. This led to the conclusion that oxidative mechanisms may cause or contribute to Parkinson's disease. Parkinson's disease may occur when either an external or an internal toxin selectively destroys dopaminergic neurons. An environmental risk factor such as exposure to pesticides or a toxin in the food supply is an example of the kind of external trigger that could hypothetically cause Parkinson's disease. So far no research has provided conclusive proof that a toxin is the cause of the disease.
Researchers believe that genetics sometimes plays a role in the cellular breakdown.
After studies in animals showed that mptp interferes with the function of mitochondria within nerve cells, investigators became interested in the possibility that impairment in mitochondrial DNA may be the cause of Parkinson's disease. Mitochondria is found in all animal cells that convert the energy in food into fuel for the cells. This theory is supported by the fact that the loss of antioxidative protective mechanisms is associated with both Parkinson's disease and increasing age. In rare instances, Parkinson's disease may be caused by a viral infection . Many researchers believe that a combination of oxidative damage, environmental toxins, genetic predisposition, and accelerated aging may ultimately be shown to cause the disease.