It remains to be understood, however, if c-reactive protein is a risk factor for this neurodegenerative disorder, or if the disease itself triggers an inflammatory response.
The study, “C-reactive Protein and Risk of Parkinson’s Disease: A Systematic Review and Meta-analysis” was published in Frontiers in Neurology.
Chronic neuroinflammation is a hallmark of Parkinson’s disease (PD). Studies have suggested that inflammatory processes may contribute to disease risk and progression, although this biological response is unlikely to be the primary cause of neuronal death.
Evidence indicates that high c-reactive protein (CRP) levels are strongly correlated with the inflammatory process. Indeed, some studies suggest a link between CRP and chronic inflammatory and neurodegenerative disorders, such as cardiovascular disease, Alzheimer’s disease, or Parkinson’s.
Although some population-based studies have explored the relationship between c-reactive protein levels and Parkinson’s risk, results so far have been contradictory.
That led researchers at the First Affiliated Hospital of Guangxi Medical University, in China, to analyze all available studies regarding c-reactive protein levels in the serum, plasma, blood, and cerebrospinal fluid — the liquid that surrounds the brain and spinal cord — in Parkinson’s patients.
Investigators searched the records of seven life sciences, biomedical or medical databases — three of them Chinese — up through October 2018, examining associations between c-reactive protein levels and Parkinson’s risk.
The team analyzed a total of 23 case-control studies published between 2009 and 2018, which involved 2,646 Parkinson’s patients (mean age 63.6–73.2) and 1,932 controls. Disease duration ranged from 3 months to 9.8 years.
Whether studies used standard or more sensitive immunoassays — a procedure used to measure certain immune-related proteins or substances — c-reactive protein concentration in whole blood, serum, and cerebrospinal fluid was found to be significantly, and consistently, higher in Parkinson’s patients than in healthy controls.
Other factors, such as the patient’s medication use or other accompanying diseases, also may affect c-reactive protein levels, the researchers said.
Although the findings indicate a link between c-reactive protein levels and Parkinson’s, it is still unknown whether this “measurable” biochemical inflammation contributes to, or is a consequence of, Parkinson’s-related neurodegenerative mechanisms.
“[T]here is growing evidence that support an association between neuroinflammation and the initiation and progression of PD pathophysiology,” the researchers wrote.
“The results of this review only suggested a correlation between CRP levels and PD, but could not completely delineate whether inflammation plays a causal role in PD, or if PD leads to inflammatory processes,” they concluded.