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Pharmaceuticals 2018, 11(4), 129;

Brain Iron Homeostasis: A Focus on Microglial Iron

Department of Genetics and Complex Diseases, Harvard TH Chan School of Public Health, Boston, MA 02115, USA
Author to whom correspondence should be addressed.
Received: 17 October 2018 / Revised: 16 November 2018 / Accepted: 19 November 2018 / Published: 23 November 2018
(This article belongs to the Special Issue Iron as Therapeutic Targets in Human Diseases)
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Iron is an essential trace element required for important brain functions including oxidative metabolism, synaptic plasticity, myelination, and the synthesis of neurotransmitters. Disruptions in brain iron homeostasis underlie many neurodegenerative diseases. Increasing evidence suggests that accumulation of brain iron and chronic neuroinflammation, characterized by microglia activation and secretion of proinflammatory cytokines, are hallmarks of neurodegenerative disorders including Alzheimer’ s disease. While substantial efforts have led to an increased understanding of iron metabolism and the role of microglial cells in neuroinflammation, important questions still remain unanswered. Whether or not increased brain iron augments the inflammatory responses of microglial cells, including the molecular cues that guide such responses, is still unclear. How these brain macrophages accumulate, store, and utilize intracellular iron to carry out their various functions under normal and disease conditions is incompletely understood. Here, we describe the known and emerging mechanisms involved in microglial cell iron transport and metabolism as well as inflammatory responses in the brain, with a focus on AD. View Full-Text
Keywords: Alzheimer’s disease; neuroinflammation; neurodegeneration; cytokines; neuroimmune responses Alzheimer’s disease; neuroinflammation; neurodegeneration; cytokines; neuroimmune responses

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Nnah, I.C.; Wessling-Resnick, M. Brain Iron Homeostasis: A Focus on Microglial Iron. Pharmaceuticals 2018, 11, 129.

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