DALLAS Sept. 12, 2006 Blocking one of the body's natural inflammatory factors gives substantial protection against cell death in the brain associated with Parkinson's disease, researchers at UT Southwestern Medical Center have found in a study on rats.
By using a drug against an inflammatory molecule called tumor necrosis factor or TNF, the researchers saw a 50 percent drop in dopamine neuron death in the brains of rats injected with compounds that cause Parkinson's-like cell death.
"Our findings suggest that TNF-dependent inflammation may be part of the progressive features of Parkinson's disease, and this gives us an opportunity with anti-TNF therapy to slow down or prevent the progression of the disease," said Dr. Mal Tansey, assistant professor of physiology at UT Southwestern and senior author of the study. "Our prediction is that independent of the environmental toxin or trigger that induces its production in the midbrain, TNF is likely to be a common mediator of dopamine neuron death."
The research will appear online and in the Sept. 13 issue of the Journal of Neuroscience.
Tumor necrosis factor is necessary for a functioning immune system. Its effects include the local inflammation and redness around wounds, and the painful swelling around joints in rheumatoid arthritis. TNF also activates other cells including cells in the brain called microglia that eat bacteria and other pathogens.
While the results point in a direction for treating neurodegenerative diseases with anti-inflammatories, a few problems will need to be addressed before anti-TNF therapies could come into widespread use to fight neurodegeneration, Dr. Tansey said. For instance, commercially available anti-TNF drugs as well as the new drug used in this study are too large to independently cross from the bloodstream into brain tissue.
Parkinson's disease affects 5 percent of people over 65, and is the second most common neuro
Contact: Aline McKenzie
UT Southwestern Medical Center