Parkinson’s, oxidative stress and inflammation

In recent years, there has been considerable interest in the role of oxidative stress (or free-radical damage) and how the body responds to inflammation, in the brains of people with Parkinson’s.  These ‘stressor’ factors create an environment which is not conducive to normal function and signs of oxidative damage have been shown to appear long before nerve 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 cell 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 abnormal mitochondrial activity and increased oxidative stress, in the cause, development and effects of Parkinson’s. Mitochondria are small structures inside cells that are responsible for energy production. A complex interplay occurs between mitochondria and other cellular processes that affect cell survival, as mitochondria are also the main cellular source of waste products. There is also a plausible link between oxidative damage and the formation of abnormal aggregates of protein that are characteristic of Parkinson’s; oxidative damage is believed to have a role in alpha-synuclein clumping and impairment of the proper breakdown of these proteins.

There is now a great deal of research going on to explore methods of reducing the inflammation response in an effort to restrict the potential damage inflicted, and this, in turn, has led to a number of clinical trials.