The recent experimental evidence that associates copper deficiency and the formation of superoxide dismutase 1 (SOD1) aggregates with the progression of PD is also discussed together with its therapeutic implication. In the present review, we describe the molecular mechanisms through which copper can exert its toxicity, by considering how it can interfere with other cellular processes known to play a role in PD, such as dopamine metabolism, oxidative stress, and α-synuclein aggregation. Alterations in copper homeostasis might have deleterious consequences, and several neurodegenerative disorders, including Parkinson’s disease (PD), have been associated with impaired copper levels. The involvement of copper in numerous physiological processes makes this metal ion essential for human life.
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