ABSTRACT
The ability of intranigral iron injection to initiate degeneration of dopamine neurons, the reduction of striatal dopamine content, the altered behavioral responses evident at higher iron dosage suggest that iron could be the cytotoxin responsible for the degeneration of nigrostriatal dopamine neurons. The nigrostriatal dopamine neurons of basal ganglia are very sensitive to chemical insult, some of which are endogenous in origin. The ability of iron chelators to displace iron from melanin predicts that future therapeutic approaches for Parkinson's disease may include the use of metal chelators in fashion similar to that used for the treatment of Wilson's disease. Therapeutic use of iron chelators, with the ability of crossing the blood-brain barrier, as agents for retarding the oxidative stress, Parkinson's disease is envisaged. The interaction of iron with melanin, the excessive accumulation of this metal in the Substantia nigra, and the increase of lipid peroxidation go some way to explain the selectivity and vulnerability of melaninized dopamine neurons to neurodegeneration.
