Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology
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 co...
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2018-01-01
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Series: | Oxidative Medicine and Cellular Longevity |
Online Access: | http://dx.doi.org/10.1155/2018/2850341 |
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doaj-b34d4867bf8545759720ccbf8f016ca52020-11-24T23:57:51ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942018-01-01201810.1155/2018/28503412850341Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide PathologyRomina María Uranga0Gabriela Alejandra Salvador1Instituto de Investigaciones Bioquímicas de Bahía Blanca, Universidad Nacional del Sur (UNS)-Consejo Nacional de Investigaciones Científicas y Técnicas, Bahía Blanca 8000, ArgentinaInstituto de Investigaciones Bioquímicas de Bahía Blanca, Universidad Nacional del Sur (UNS)-Consejo Nacional de Investigaciones Científicas y Técnicas, Bahía Blanca 8000, ArgentinaIron 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.http://dx.doi.org/10.1155/2018/2850341 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Romina María Uranga Gabriela Alejandra Salvador |
spellingShingle |
Romina María Uranga Gabriela Alejandra Salvador Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology Oxidative Medicine and Cellular Longevity |
author_facet |
Romina María Uranga Gabriela Alejandra Salvador |
author_sort |
Romina María Uranga |
title |
Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology |
title_short |
Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology |
title_full |
Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology |
title_fullStr |
Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology |
title_full_unstemmed |
Unraveling the Burden of Iron in Neurodegeneration: Intersections with Amyloid Beta Peptide Pathology |
title_sort |
unraveling the burden of iron in neurodegeneration: intersections with amyloid beta peptide pathology |
publisher |
Hindawi Limited |
series |
Oxidative Medicine and Cellular Longevity |
issn |
1942-0900 1942-0994 |
publishDate |
2018-01-01 |
description |
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. |
url |
http://dx.doi.org/10.1155/2018/2850341 |
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