Measuring blood levels of the signaling molecule CXCL12 and its receptor CXCR4 may help identify active inflammation in Parkinson’s disease patients, a study suggests.
The study, “CXCL12 and CXCR4 in the Peripheral Blood of Patients with Parkinson’s Disease,” was published in Neuroimmunomodulation.
CXCL12 is a small protein called a chemokine that triggers immune cells to the site of inflammation where they can exert their pro-inflammatory activity.
Previous studies have shown that CXCL12 proteins are increased in inflammatory diseases including inflammatory bowel disease and rheumatoid arthritis, and inhibiting its receptor, CXCR4, may hold therapeutic potential for these diseases.
In addition, CXCL12 has also been shown to contribute to the development of neurodegenerative disorders, such as multiple sclerosis. Preventing the migration of immune cells to lesion sites in the brain could block the progression of such damaging disorders.
“These observations reinforce the significant role of the CXCL12/CXCR4 axis in inflammatory responses,” the researchers wrote.
Parkinson’s disease is characterized by reduced levels of dopamine in the brain caused by the death of dopamine-producing nerve cells. Although it is not fully understood what promotes the death of this particular subset of brain cells, several studies have demonstrated that oxidative stress — cellular damage as a consequence of high levels of oxidant molecules — and increased inflammation are critical players.
Iranian researchers have now investigated the role of CXCL12 and its receptor in Parkinson’s disease.
They evaluated blood samples collected from 30 patients with confirmed Parkinson’s disease and 40 age- and sex-matched healthy volunteers. The patients had the disease for a mean duration of 4.17 years.
The analysis revealed that levels of CXCL12 were 2.4 times higher in Parkinson’s patients over the control group. In addition, CXCR4 levels in peripheral blood mononuclear cells (PBMC, consisting of major immune cells, like T- and B-cells) were found to be approximately three times higher in Parkinson’s patients.
Based on these findings, the researchers believe that CXCL12 signals mediated by CXCR4 could contribute to the activation of immune cells, inflammation, and neurotoxicity linked to Parkinson’s disease.
Importantly, “CXCR4 expression in PBMC or CXCL12 serum levels may be potential biomarkers of inflammation in PD [Parkinson’s disease] patients,” the researchers wrote.
However, the team notes that some studies have found contrasting results, suggesting that CXCL12 signals could be protective for the central nervous system. This highlights the need for further studies to clarify the exact role of CXCL12/CXCR4 signals in the progression of Parkinson’s disease.