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Mitoch. Fe, Cu, glutathione in PD

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    Neurochem Int. 2017 May 31. pii: S0197-0186(17)30250-4. doi: 10.1016/j.neuint.2017.05.016. [Epub ahead of print]
    Nexus between mitochondrial function, iron, copper and glutathione in Parkinson's disease.

    Liddell JR1, White AR2.
    Author information

    1
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia. Electronic address: [email protected].
    2
    Cell and Molecular Biology, QIMR Berghofer Medical Research Institute, Herston, Queensland 4006, Australia.
    Abstract

    Parkinson's disease is neuropathologically characterised by loss of catecholamine neurons in vulnerable brain regions including substantia nigra pars compacta and locus coeruleus. This review discusses how the susceptibility of these regions is defined by their shared biochemical characteristics that differentiate them from other neurons. Parkinson's disease is biochemically characterised by mitochondrial dysfunction, accumulation of iron, diminished copper content and depleted glutathione levels in these regions. This review also discusses this neuropathology, and provides evidence for how these pathological features are mechanistically linked to each other. This leads to the conclusion that disruption of mitochondrial function, or iron, copper or glutathione metabolism in isolation provokes the pathological impairment of them all. This creates a vicious cycle that drives pathology leading to mitochondrial failure and neuronal cell death in vulnerable brain regions.
 
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