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Iron elevations in the aging Parkinsonian brain: a consequence of impaired iron homeostasis?
Author(s) -
Lee Donna W.,
Andersen Julie K.
Publication year - 2010
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2009.06470.x
Subject(s) - iron homeostasis , homeostasis , neuroscience , parkinson's disease , biology , disease , chemistry , microbiology and biotechnology , metabolism , biochemistry , medicine
The contribution of iron dysregulation to the etiology of a variety of neuronal diseases comes as no surprise given its necessity in numerous general cellular and neuron‐specific functions, its abundance, and its highly reactive nature. Homeostatic mechanisms such as the iron regulatory protein and hypoxia‐inducible factor pathways are firmly evolutionarily set in place to prevent ‘free’ iron from participating in chemical Fenton and Haber‐Weiss reactions which can result in subsequent generation of toxic hydroxyl radicals. However, given the multiple layers of complexity in cellular iron regulation, disruption of any number of genetic and environmental components can disturb the delicate balance between the various molecular players involved in maintaining an appropriate metabolic iron homeostasis. In this review, we will primarily focus on: (i) the impact of aging and gender on iron dysfunction as these are important criteria in the determination of iron‐related disorders such as Parkinson’s disease (PD), (ii) how iron mismanagement via disruption of cellular entry and exit pathways may contribute to these disorders, and (iii) how the availability of non‐invasive measurement of brain iron may aid in PD diagnosis.