Iron, Neuroinflammation and Neurodegeneration

Disturbance of the brain homeostasis, either directly via the formation of abnormal proteins or cerebral hypo-perfusion, or indirectly via peripheral inflammation, will activate microglia to synthesise a variety of pro-inflammatory agents which may lead to inflammation and cell death. The pro-inflam...

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Main Authors: Roberta J. Ward, David T. Dexter, Robert R. Crichton
Format: Article
Language:English
Published: MDPI AG 2022-06-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/13/7267
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author Roberta J. Ward
David T. Dexter
Robert R. Crichton
author_facet Roberta J. Ward
David T. Dexter
Robert R. Crichton
author_sort Roberta J. Ward
collection DOAJ
description Disturbance of the brain homeostasis, either directly via the formation of abnormal proteins or cerebral hypo-perfusion, or indirectly via peripheral inflammation, will activate microglia to synthesise a variety of pro-inflammatory agents which may lead to inflammation and cell death. The pro-inflammatory cytokines will induce changes in the iron proteins responsible for maintaining iron homeostasis, such that increased amounts of iron will be deposited in cells in the brain. The generation of reactive oxygen and nitrogen species, which is directly involved in the inflammatory process, can significantly affect iron metabolism via their interaction with iron-regulatory proteins (IRPs). This underlies the importance of ensuring that iron is maintained in a form that can be kept under control; hence, the elegant mechanisms which have become increasingly well understood for regulating iron homeostasis. Therapeutic approaches to minimise the toxicity of iron include N-acetyl cysteine, non-steroidal anti-inflammatory compounds and iron chelation.
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spelling doaj.art-648481e5abe547e592201e343accc3802023-11-23T20:10:50ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-06-012313726710.3390/ijms23137267Iron, Neuroinflammation and NeurodegenerationRoberta J. Ward0David T. Dexter1Robert R. Crichton2Department of Medicine, Imperial College, London SW7 2AZ, UKDepartment of Medicine, Imperial College, London SW7 2AZ, UKSchool of Chemistry, University Catholique de Louvain, 1348 Louvain-la-Neuve, BelgiumDisturbance of the brain homeostasis, either directly via the formation of abnormal proteins or cerebral hypo-perfusion, or indirectly via peripheral inflammation, will activate microglia to synthesise a variety of pro-inflammatory agents which may lead to inflammation and cell death. The pro-inflammatory cytokines will induce changes in the iron proteins responsible for maintaining iron homeostasis, such that increased amounts of iron will be deposited in cells in the brain. The generation of reactive oxygen and nitrogen species, which is directly involved in the inflammatory process, can significantly affect iron metabolism via their interaction with iron-regulatory proteins (IRPs). This underlies the importance of ensuring that iron is maintained in a form that can be kept under control; hence, the elegant mechanisms which have become increasingly well understood for regulating iron homeostasis. Therapeutic approaches to minimise the toxicity of iron include N-acetyl cysteine, non-steroidal anti-inflammatory compounds and iron chelation.https://www.mdpi.com/1422-0067/23/13/7267neuroinflammationiron homeostasismicrogliaastrocytesiron
spellingShingle Roberta J. Ward
David T. Dexter
Robert R. Crichton
Iron, Neuroinflammation and Neurodegeneration
International Journal of Molecular Sciences
neuroinflammation
iron homeostasis
microglia
astrocytes
iron
title Iron, Neuroinflammation and Neurodegeneration
title_full Iron, Neuroinflammation and Neurodegeneration
title_fullStr Iron, Neuroinflammation and Neurodegeneration
title_full_unstemmed Iron, Neuroinflammation and Neurodegeneration
title_short Iron, Neuroinflammation and Neurodegeneration
title_sort iron neuroinflammation and neurodegeneration
topic neuroinflammation
iron homeostasis
microglia
astrocytes
iron
url https://www.mdpi.com/1422-0067/23/13/7267
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AT davidtdexter ironneuroinflammationandneurodegeneration
AT robertrcrichton ironneuroinflammationandneurodegeneration