In recent years, there has been some considerable interest in the role of free-radical damage or oxidative stress and how the body responds to inflammation, in the Parkinsonian brain. These ‘stressor’ factors create an environment in the brain which is not conducive to normal function and signs of oxidative damage have been shown to appear long before brain cells (neurons) actually degenerate in Parkinson’s:
Oxidative stress is essentially an imbalance between the production of highly chemically reactive substances in cells and the ability of the body to counteract or detoxify their harmful effects, resulting in cell damage or death.
Inflammation is the body’s attempt at self-healing; the aim being to remove harmful substances, including damaged or degenerated cells and begin the healing process. When something harmful affects a part of the body, the biological response to try to remove it results in the signs and symptoms of inflammation.
Strong evidence now exists to support a role for abnormal mitochondrial activity and increased oxidative stress, in the cause, development and effects of Parkinson’s. A complex interplay occurs between mitochondria and other cellular complexes that affects cell survival, as mitochondria not only have a key role in cell energy production, but they are also the main cellular source of waste products.
There is a plausible link between oxidative damage and the formation of abnormal aggregates of protein that are characteristic of Parkinson’s; oxidative damage, it is thought, induces alpha-synuclein clumping and impairs the proper degradation of the proteins.