Posted by: Glow-worm PJ9 FEB 2012
Parkinson’s disease attacks the substantia nigra of the brain, which is responsible for the control of movement. In Parkinson’s sufferers, damage to the mitochondria in the dopaminergic neurones of the brain, along with a build-up of harmful by-products, causes depletion of these neurones.
There has been some uncertainty as to whether mitochondrial damage is a cause or a consequence of Parkinson’s disease, but research into two genes known to be involved in the disease, called parkin and PINK1, has supported the idea that mitochondrial damage plays a causative role in the disease. Cells deficient in either protein have abnormal mitochondria. The parkin gene is recruited to damaged mitochondria to aid their destruction, but the process is dependent upon the presence of PINK1. It was found that giving the cells extra PINK1 led to increased parkin recruitment and mitochondrial destruction.
Other research studied the effect of parkin on larvae of the fruit fly Drosophila. They showed a marked decrease in speed, and slower muscle contractions, reminiscent of bradykinesia. It was also discovered that levels of adenosine triphosphate, and therefore energy production, was decreased, with an increase in lactate levels. The parkin larvae also showed oxidative stress caused by high levels of free radicals.
Further research carried out at Cambridge University has centred upon the fact that viruses often stabilise mitochondria in cells they infect in order to increase the cell’s chances of survival as a host. A viral protein was injected into rats with Parkinson’s-like brain lesions, and it was discovered they performed better in tests involving motor function, and their brains were found to contain more dopaminergic neurones.
Much remains unclear about the role of neuronal mitochondria in the development of Parkinson’s disease, but it gives hope for future management of the disease.