Iron is one of the foundational minerals required by the human body, used to bind oxygen in hemoglobin, for energy production in mitochondria, as well as for countless other necessary processes. In the brain, iron is vital for the myelination of axons, providing insulation for the transmission of signals necessary to the functioning of this capstone organ. However, excess of iron is known to cause inflammation and is implicated in the neurodegeneration seen in various brain disorders, particularly Parkinson’s disease. To prevent this overload from occurring, a highly regulated, robust mechanism has evolved to control the storage, release, and transport of iron throughout various tissues. This mechanism is especially crucial in the brain, which must remain vigilant to the threat of iron overload and the associated cellular damage. However, it remains to be seen how exactly this process results in the specific pattern of iron accumulation which is seen in the deep nuclei of the aging brain. This question has important implications for the study of neurodegenerative disorders and the associated iron overload.
In response to this question, we have three research aims. First, we wish to build a spatiotemporal atlas of brain iron accumulation based on MRI data. Second, we will use this atlas to investigate the relationship between iron accumulation in deep gray nuclei and gene expression. This analysis will yield insight into the mechanism behind the process of iron transport in the brain, and how that changes with normal ageing. Finally, we will investigate the relationship between iron accumulation and health outcomes. Understanding how iron concentration evolves in the human brain will help characterize the processes involved in brain development and ageing. This research will be equally useful for the study of iron related neurological disorders like Parkinson’s disease.