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.