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Disease Mechanisms in Neuroscience

It has been known for several years that iron levels within the substantia nigra are elevated in Parkinson’s disease. Because accessible ferrous iron (Fe) can react with hydrogen peroxide to generate hydroxyl radicals, it is possible that the increases in iron within the substantia nigra play a causal role, contributing to neuronal degeneration in Parkinson’s disease. However, it is also possible that increased iron levels are a consequence of neuronal degeneration, and the role of iron thus has remained controversial. Now, Kaur and others (2003) have presented evidence that suggests that elevated iron may play a causal role. In one set of experiments, these investigators examined the effects of iron chelation via the expression of the iron-binding protein ferritin in transgenic mice and observed decreased susceptibility to the Parkinson’s-inducing agent MPTP. In a second line of experiments, the metalchelating agent clioquinol was administered. Again, there was protection against the effects of MPTP. This study, which demonstrates reduction in reactive iron via genetic and pharmacological interventions, provides evidence for a role of iron in the pathogenesis of Parkinson’s disease. There is clearly a need for additional studies on the actions of iron in the brain. If future investigations confirm a role in the pathophysiology of substantia nigra degeneration, the authors’ suggestion, that iron chelation may provide a therapeutic approach in Parkinson’s disease, will be strengthened.