Cited by 151Iron Metabolism and DisordersNeurological diseases and metabolismNeuroinflammation and Neurodegeneration Mechanisms

Iron deposits in the chronically inflamed central nervous system and contributes to neurodegeneration

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Andersen, Hjalte Holm, Johnsen, Kasper Bendix, Moos, Torben·2014·Cellular and Molecular Life Sciences

Abstract

Neurodegenerative disorders are characterized by the presence of inflammation in areas with neuronal cell death and a regional increase in iron that exceeds what occurs during normal aging. The inflammatory process accompanying the neuronal degeneration involves glial cells of the central nervous system (CNS) and monocytes of the circulation that migrate into the CNS while transforming into phagocytic macrophages. This review outlines the possible mechanisms responsible for deposition of iron in neurodegenerative disorders with a main emphasis on how iron-containing monocytes may migrate into the CNS, transform into macrophages, and die out subsequently to their phagocytosis of damaged and dying neuronal cells. The dying macrophages may in turn release their iron, which enters the pool of labile iron to catalytically promote formation of free-radical-mediated stress and oxidative damage to adjacent cells, including neurons. Healthy neurons may also chronically acquire iron from the extracellular space as another principle mechanism for oxidative stress-mediated damage. Pharmacological handling of monocyte migration into the CNS combined with chelators that neutralize the effects of extracellular iron occurring due to the release from dying macrophages as well as intraneuronal chelation may denote good possibilities for reducing the deleterious consequences of iron deposition in the CNS.

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  1. [90]Zacharski LR Gerhard GS Atherosclerosis: a manifestation of chronic iron toxicity? Vasc Med 2003 8 153 155 14989554

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Authors
Andersen, H. H., Johnsen, K. B., & Moos, T.
Affiliations
Aalborg University (DK)
Corresponding author
Moos, Torben
Venue
Cellular and Molecular Life Sciences
Published
2013-11-12
Volume
71
Issue
9
Pages
1607-1622
ISSN
  • 1420-682X (ISSN-L)
  • 1420-9071
OpenAlex
W2157974947
Cited by
151
References
172
Citations by year
2026: 9 · 2025: 6 · 2024: 11 · 2023: 10 · 2022: 12 · 2021: 21 · 2020: 12 · 2019: 13 · 2018: 13 · 2017: 11 · 2016: 10 · 2015: 17 · 2014: 6
FWCI
1.68
Type
journal article
Language
en
Open access
Locations
  • Cellular and Molecular Life Sciences (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • VBN Forskningsportal (Aalborg Universitet) (submittedVersion, other-oa)
Funders
  • Lundbeckfonden
  • H. Lundbeck A/S
Topics
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
  • Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
iron accumulation, neuroinflammation, neurodegeneration, monocyte migration, macrophages, labile iron, oxidative stress, free radicals, glial cells, phagocytosis, iron chelators, neurodegenerative diseases
MeSH terms
Central Nervous System, Ferritins, Free Radicals, Humans, Iron, Iron Chelating Agents, Macrophages, Oxidative Stress, Neurodegenerative Diseases

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