The levels of two proteins known as APOC1 and autotaxin are increased in the cerebral spinal fluid of people with fibromyalgia and neuropathic pain, a study has found.
Results of the study, “CSF levels of apolipoprotein C1 and autotaxin found to associate with neuropathic pain and fibromyalgia,” suggest that these proteins could take part in underlying pain mechanisms involved in these disorders. However, additional studies are still warranted to better understand their role.
Conducted by researchers at Swedish and Norwegian institutions, the study was published in the Journal of Pain Research.
The team analyzed cerebral spinal fluid (CSF) samples collected from a total of 65 patients, of whom 40 had fibromyalgia and 25 had neuropathic pain, and from 134 volunteers, of whom 11 were healthy and the remaining had had minor urology surgery.
First, the researchers performed an analysis of the levels of 55 proteins, which had been previously reported to be linked to pain modulation through spinal cord stimulation.
They identified a subset of 10 proteins that were significantly altered in CSF samples of patients with neuropathic pain; of these, the ones that showed a stronger association were apolipoprotein C-I (APOC1), keratin 1 (KRT1), apolipoprotein A1 (APOA1), and neurexin-1 (NRXN1).
In patients with fibromyalgia, the autotaxin protein (also referred to as ENPP2) showed more differences than controls. This protein was also found to be higher in CSF samples of fibromyalgia patients than in those with neuropathic pain.
A total of 14 participants who had long-lasting neuropathic pain (median of 10 years) had a spinal cord stimulator (SCS) permanently implanted for managing their symptoms. They reported significant pain relief after the procedure.
Based on the positive effect of the treatment, the team analyzed the protein CSF content in these patients before and after the surgery aiming to find a biomarker that could be linked to pain modulation.
The analysis did not reveal any significant differences in protein content between the two CSF sample sets (before and after the procedure). However, when compared with the controls, neuropathic pain patients showed higher levels of APOC1 and secretogranin-1 while off SCS treatment.
“The increased levels of APOC1 and ENPP2 found in neuropathic pain and fibromyalgia patients may shed light on the underlying mechanisms of these conditions,” the researchers wrote.
More research is needed on how these proteins may contribute to both fibromyalgia and ENPP2 pain symptoms.
APOC1 is known to be able to modulate inflammatory responses, and has been found to mediate important cell-activating mechanisms involved in neuropathic pain in mice. ENPP2, on the other hand, has been previously linked to nerve cell health and pinpointed as an important regulator of spinal signal processing.
“Available literature supports the involvement of [APOC1 and ENPP2] in both neuropathic pain and fibromyalgia,” and “supports further investigation of these proteins and their mediators to determine their potential role in human pain pathophysiology [development],” the researchers concluded.