A new finding may shed more light on the role of inflammation in Parkinson's disease--a progressive degenerative disease marked by decreased levels of dopamine in the brain.
Researchers at the University of Texas Health Science Center at Houston found that a single, high-dose exposure of an experimental inflammatory agent in an animal model triggers changes in brain tissue that resemble Parkinson's in humans.
While the exact cause of Parkinson's is still unknown, scientists believe that the beginning of neurodegeneration is connected to an inflammatory event or episode and that further loss of dopaminergic neurons leads to chronic neuroinflammation. A better understanding of inflammation and its link to loss of dopamine--which is involved in sending messages to the part of the brain that controls coordination and movement--could eventually help scientists find better therapies for the disease.
Rats with an animal form of Parkinson's that mimics many of the neuropathic changes associated with the disease were given lipopolysaccharide (LPS) or a control saline solution. Researchers euthanized the rats after 48 hours, then removed the rat brains. They found that a single injection of LPS caused an asystemic inflammatory response in the rats and raised certain circulatory cytokines--small signaling molecules. In tissue taken from the olfactory bulb, researchers found immune-associated cells, and individual cytokines within the olfactory bulb had increased levels of certain types of cytokines. Essentially, the single dose of LPS produced an inflammatory response that closely resembled the characteristics of Parkinson's development.
The study was presented last week at the Experimental Biology 2013 meeting in Boston and will appear in an upcoming issue of the Journal of Interferon & Cytokine Research.
The investigators say the research suggests that not only does inflammation initiate an immune response in Parkinson's patients, but that persistent and more frequent pro-inflammatory mechanisms give rise to dopaminergic neuron death as cellular protective mechanisms are weakened.
- read the press release