Iron is probably as old as the universe itself and is essential for sustaining biological processes. The remarkable property of iron complexes to facilitate electron transfer makes it a significant component of redox reactions that drive the essential steps in nucleic acid biosynthesis and cellular functions. This, however, also generates potentially harmful hydroxyl radicals causing cell damage. In the movement disorder world, iron accumulation is well known to occur in neurodegeneration with brain iron accumulation, while dysfunctional iron homeostasis has been linked with neurodegenerative diseases like Parkinson’s disease and Huntington’s disease to name a few. Targeting excess iron in these patients with chelation therapy has been attempted over the last few decades, though the results have not been that promising. In this review, we have discussed iron, its metabolism, and proposed mechanisms causing movement disorder abnormalities. We have reviewed the available literature on attempts to treat these movement disorders with chelation therapy. Finally, based on our understanding of the pathogenic role of iron, we have critically analyzed the limitations of chelation therapy in the current scenario and the various unmet needs that should be addressed for selecting the patient population amenable to this therapy.
