Iron deposits in the chronically inflamed central nervous system and contributes to neurodegeneration
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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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Elevated iron in the CNS is associated with ND, possibly at levels higher than with normal aging.
“Indeed, elevated iron in the CNS is associated with ND (reviewed in [133] and [134]), possibly at levels higher than with normal aging [133].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [133]
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- [90]Zacharski LR Gerhard GS Atherosclerosis: a manifestation of chronic iron toxicity? Vasc Med 2003 8 153 155 14989554
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Interactions of iron, dopamine and neuromelanin pathways in brain aging and Parkinson's disease
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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
- PMC
- PMC3983878
- 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
- hybrid
- doi.org
- 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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