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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 2850341, 12 pages
Review Article

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

1Instituto de Investigaciones Bioquímicas de Bahía Blanca, Universidad Nacional del Sur (UNS)-Consejo Nacional de Investigaciones Científicas y Técnicas, Bahía Blanca 8000, Argentina
2Departamento de Biología, Bioquímica y Farmacia, UNS, Bahía Blanca 8000, Argentina

Correspondence should be addressed to Romina María Uranga; ra.ude.abirc@agnarur and Gabriela Alejandra Salvador; ra.ude.abirc@rodavlas

Received 12 October 2017; Accepted 17 December 2017; Published 31 January 2018

Academic Editor: Daiana S. Avila

Copyright © 2018 Romina María Uranga and Gabriela Alejandra Salvador. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 (Aβ) and iron, will be summarized.