Iron and Neurodegeneration

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Background

As a co-factor of several proteins, iron is involved in essential biological processes in the central nervous system (CNS), from oxygen transport to mitochondrial respiration, myelination and synthesis of neurotransmitters.

Both iron deficiency, through decreased activity of iron-dependent proteins, and iron excess, by means of neurotoxic mechanisms, may result in harmful effects in the CNS. Hence, iron homeostasis is finely regulated through the control of iron exchange across the blood-brain barrier and the synchronized expression and management of proteins, involved in iron uptake, storage, mobilization, trafficking and exit, in all CNS cells.

Iron deficiency is implicated in developmental cognitive dysfunctions, while iron overload or dyshomeostasis is observed in brain aging and neurodegenerative disorders, like Alzheimer’s, Parkinson’s and Huntington’s diseases, -synucleinopathies, taupathies, Lysosomal Storage Disorders, Amyotrophic Lateral Sclerosis, Frontotemporal Dementia, Neurodegenerations with Brain Iron Accumulation, Friedreich’s ataxia and Multiple Sclerosis. Given the huge etiopathogenetic differences in these pathologies, iron imbalance most likely occurs and acts in distinct pathways and different CNS cells. Nonetheless, common denominators may be identified as major drivers or consequences of brain iron homeostasis disruption in neurodegenerative disorders.

Iron dyshomeostasis, protein aggregation and impaired autophagy are common hallmarks of several neurodegenerative diseases. It is noteworthy that iron mobilization from the main cellular iron-storage protein, i.e. ferritin, occurs through a macroautophagic pathway, named ferritinophagy. Ferroptosis is implicated in neuronal loss in many neurodegenerative disorders and its induction leads to ferritinophagy activation and iron release. Amyotrophic Lateral Sclerosis-associated mutations in TBK1 gene result in defective ferritinophagy. Further, iron accumulation in senescent cells is associated with impaired ferritinophagy.

Neuroinflammation and immunity are also emerging as central actors in the pathogenesis of many neurodegenerative diseases. Iron metabolism, inflammation and immunity are tightly interlinked. Iron affects macrophage and microglia polarization versus iron-sequestering M1 pro-inflammatory or iron-releasing M2 anti-inflammatory cells. Hepcidin, the liver-derived master regulator of systemic iron homeostasis, also acts on and is produced by many cells in the CNS. It increases with aging in the brain and, being a mediator of innate immunity, is induced by neuroinflammation. Hepcidin effects in the CNS are however controversial, since it has been shown both to mediate neuroinflammation or iron dyshomeostasis and to attenuate pro-inflammatory responses or decrease iron overload.

In many neurodegenerative disorders, neurotoxic aggregated proteins are present in exosomes and spread from cell to cell through extracellular vesicles. Some neurotoxic proteins can bind and interact with iron. Further, many proteins, involved in iron uptake, storage and release, function on the plasma membrane, traffic between intracellular compartments within vesicles and are found in extracellular vesicles. These observations suggest a potential role of extracellular vesicles in CNS iron dyshomeostasis.

To provide a more comprehensive overview of the role of iron in neurodegeneration, we invite any type of contribution (original research manuscripts, reviews, perspectives), exploring, but not limited to, the aforementioned subtopics. Contributions from all research areas, including disease modelling, human neuropathology, biochemical, molecular and clinical studies, genomics, proteomics or therapeutic interventions are welcome.

Keywords: iron, neurodegeneration, autophagy, neuroinflammation, exosomes

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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