A University of South Florida study has suggested that targeting the neuroinflammatory causes Parkinson's disease with a brain chemical signal may lead to better understanding of the disease and pave way for better therapies.
Brain inflammation has been clearly shown in PD, and the brain's microglia-small cells that regulate the chemical environment of neural cells-play a role in the inflammatory process and disease progression, said study lead author Paula C. Bickford.
"In the brain, one aspect of immune regulation occurs through neurons. Immune cells called microglia can damage neurons by producing bioactive molecules. On the other hand, a neuron-generated signaling chemical, or fractalkine, also called CX3CL1, suppresses the activation of microglia.
"Our study examined whether adding CX3CL1 beyond normal levels could decrease microglial activation and, therefore, play a neuroprotective role by helping prevent the loss of important neural cells in an animal model of Parkinson's disease," said Bickford.
Using rat models of Parkinson's with known inflammatory components, the researchers added CX3CL1 in varying doses and found that, in all cases, CX3CL1 reduced the loss of dopamine cells.
The loss of dopamine rich nerve fibers in the brain is a key aspect of Parkinson's, leading to movement-related symptoms such as tremors, muscle stiffness, balance problems and slowness.
"This suggests that the communication between neurons and glial cells may play a role in Parkinson's disease neurodegeneration," said Carmelina Gemma, co-lead scientist for the study.
The findings have been published online in the Journal of Neuroinflammation.