ve cells in an area of the brain called the substantia nigra. By the time serious symptoms appear, more than 80 percent of the dopamine-producing nerve cells are already dead, and the damage is irreversible.
In addition to its beneficial role, TNF has been a suspected player in Parkinson’s because elevated levels of it are found in post-mortem brains and cerebrospinal fluid of people with the disease. A previous study by other researchers found that non-steroidal anti-inflammatory drugs that block production of TNF and related molecules can reduce the risk of developing Parkinson’s by 46 percent.
In the current study, UT Southwestern researchers injected two different substances into the rats’ brains to cause cell death in the substantia nigra – low-dose infusion of LPS, a toxin from bacteria often used to mimic chronic inflammation of the central nervous system, and 6-hydroxydopamine, which kills cells by creating an overwhelming amount of reactive oxygen and nitrogen molecules. Cell death was measured by counting neurons in stained brain slices.
When an experimental TNF inhibitor called XENP345, designed specifically to block soluble TNF, was also introduced into the brain, dopamine neuron death was reduced by about half.
The same effect was found on cultured dopamine neurons exposed to either toxin.
The researchers are now looking into why TNF inhibition did not fully protect against cell death. For example, the drug may not have been able to fully diffuse throughout the tissue, it might take longer to work than the weeks allowed in the experiment, or dopamine neuron loss might also involve processes independent of TNF.
“If an intervention could still reduce the extent or rate of cell death by 50 percent, it could make a huge difference in the life of a Parkinson’s disease patient,” Dr. Tansey said.
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