Cited by 48Iron Metabolism and DisordersNeurological diseases and metabolismTrace Elements in Health

Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology

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Uranga, Romina María, Salvador, Gabriela Alejandra·2018·Oxidative Medicine and Cellular Longevity

Abstract

Iron overload is a hallmark of many neurodegenerative processes such as Alzheimer’s, Parkinson’s, and Huntington’s diseases. Unbound iron accumulated as a consequence of brain aging is highly reactive with water and oxygen and produces reactive oxygen species (ROS) or free radicals. ROS are toxic compounds able to damage cell membranes, DNA, and mitochondria. Which are the mechanisms involved in neuronal iron homeostasis and in neuronal response to iron‐induced oxidative stress constitutes a cutting‐edge topic in metalloneurobiology. Increasing our knowledge about the underlying mechanisms that operate in iron accumulation and their consequences would shed light on the comprehension of the molecular events that participate in the pathophysiology of the abovementioned neurodegenerative diseases. In this review, current evidences about iron accumulation in the brain, the signaling mechanisms triggered by metal overload, as well as the interaction between amyloid β (A β) and iron, will be summarized.

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  • When iron is present in the cytosol, dopamine can be oxidized into dopamine quinone (DAQ), which is highly reactive and toxic.

    “When iron is present in the cytosol (as may occur more frequently with ageing)265,266, dopamine can be oxidized into dopamine quinone (DAQ), which is highly reactive and toxic267,268.”

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  1. [2]Fraústo da Silva J. J. R. Williams R. J. P. The biological chemistry of the elements 2001 Oxford Oxford University Press
  2. [25]Han J. Day J. R. Connor J. R. Beard J. L. Gene expression of transferrin and transferrin receptor in brains of control vs. iron-deficient rats Nutritional Neuroscience 2003 6 1 1 10 12608731
  3. [59]Crichton R. Ward R. J. Metal-Based Neurodegeneration: From Molecular Mechanisms to Therapeutic Strategies 2014 John Wiley & Sons

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Authors
Uranga, R. M., & Salvador, G. A.
Affiliations
Consejo Nacional de Investigaciones Científicas y Técnicas (AR)
Corresponding author
  • Uranga, Romina María
  • Salvador, Gabriela Alejandra
Venue
Oxidative Medicine and Cellular Longevity
Publisher
Wiley
Published
2018-01
Volume
2018
Issue
1
Pages
2850341-2850341
ISSN
  • 1942-0994 (ISSN-L)
  • 1942-0900
OpenAlex
W2787435117
Cited by
48
References
150
Citations by year
2026: 2 · 2025: 4 · 2024: 5 · 2023: 7 · 2022: 5 · 2021: 5 · 2020: 9 · 2019: 8 · 2018: 3
FWCI
1.03
Type
journal article
Language
en
Open access
Locations
  • Oxidative Medicine and Cellular Longevity (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-sa)
  • Americanae (AECID Library) (submittedVersion, cc-by-nc-sa)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • Agencia Nacional de Promoción Científica y Tecnológica (2013-0987, 2010-936)
  • Consejo Nacional de Investigaciones Científicas y Técnicas
  • Universidad Nacional del Sur (PGI24B/179)
Topics
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
  • Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
  • Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
Keywords
iron overload, neurodegeneration, amyloid-beta, Alzheimer's disease, Parkinson's disease, Huntington's disease, oxidative stress, reactive oxygen species, iron homeostasis, brain aging
MeSH terms
Humans, Iron, Amyloid beta-Peptides, Oxidative Stress, Neurodegenerative Diseases

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