Targeting the neuroinflammatory causes of Parkinson's disease with a naturally present brain chemical signal could offer a better understanding of the clinical mechanisms of the disease and open a future therapeutic window, reports a team of researchers from the University of South Florida Department Neurosurgery and Brain Repair and the James A. Haley Veterans' Administration Hospital, Tampa.
Their findings are published online in the Journal of Neuroinflammation (http://www.jneuroinflammation).
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, PhD, professor of neurosurgery at USF and a senior research career scientist at the Haley VA Hospital.
"In the brain, one aspect of immune regulation occurs through neurons," said Dr. Bickford. "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."
Using rat models of Parkinson's with known inflammatory components, the researchers added CX3CL1 in varying doses and found that, in all cases, CX3CL1 (which has a single receptor - CX3CR1 found on microglia) 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.