Iron is essential for life and crucial to the human central nervous system (CNS). It is fundamental in biochemical pathways, including oxidative phosphorylation, myelin synthesis, neurotransmitter production and the synthesis/metabolism of serotonin and dopamine, all of which are essential for normal CNS function. Because iron is highly reactive towards oxygen in aerobic cells, maintenance of cellular iron homeostasis is vital for normal neuronal function and for overall organism viability. Unfortunately, a growing number of human neurodegenerative disorders, including Alzheimer's, Huntington's, Parkinson's, and Friedreich's ataxia, have phenotypes confirming disease associated with disruption of iron homeostasis. While it is widely accepted that inflammation associated with dysfunctional iron homeostasis, accompanied by concomitant oxidative stress, is a key factor in these neurodegenerative disorders, the molecular details regarding disease related protein malfunctions are regrettably lacking. This only highlights a need for an expanded understanding of iron regulation events in the body, as this knowledge is fundamental for the development of new therapeutic approaches in the treatment of this growing class of neurodegenerative disorders. Expanding this understanding at the molecular level is the broad goal of the Stemmler laboratory.