Oxidative stress in Parkinson's disease

Authors

  • A. H. V. Schapira

    Corresponding author
    1. Department or Clinical Neurosciences, Royal Free Hospital School of Medicine, London, UK
      Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, Rowland Hill Streel, London NW3 2PF, UK.
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Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, Rowland Hill Streel, London NW3 2PF, UK.

Abstract

Oxidative damage and mitochondrial dysfunction are now considered to be important events in the cause of dopaminergic cell death in Parkinson's disease (PD). It is not known whether these biochemical abnormalities represent primary causes of PD or whether they are the end result of a series of reactions precipitated by environmental and genetic factors. Both oxidative damage and complex 1 deficiency are linked in a reciprocal manner and can potentially produce a toxic cellular environment capable of attacking a variety of biomolecules as well as inhibiting energy production. Defining the roles that these two biochemical defects play in nigral neuronal loss will provide important insights into the aetiology of PD.

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