A recent news release indicates that Massachusetts General Hospital (MGH) investigators have found evidence of neuroinflammation in key regions of the brains of patients with chronic pain. Their study appears online in the journal Brain and may help pave the way to the exploration of potential new treatment strategies.
Marco Loggia, PhD, of the MGH-based Martinos Center for Biomedical Imaging, lead author of the report, explains that finding increased levels of the translocator protein in regions like the thalamus is key, since the protein is highly expressed in microglia and astrocytes, the immune cells of the central nervous system, when they are activated in response to some pathological event.
“Demonstrating glial activation in chronic pain suggests that these cells may be a therapeutic target, and the consistency with which we found glial activation in chronic pain patients suggests that our results may be an important step towards developing biomarkers for pain conditions,” Loggia adds.
According to the release, many studies have clearly linked glial activation with persistent pain in animal models. However, none have previously documented glial activation in the brain of humans with chronic pain. The current study encompassed a total of 19 patients with chronic lower back pain and 25 health control participants. The release notes that in a subset of 10 patients and 9 pain-free controls, brain imaging studies were conducted with one of the Martinos Center’s integrated PET/MR scanners using a new radiopharmaceutical that binds to the translocator protein (TSPO). The researchers observed that the levels of the protein in the thalamus and other brain regions were significantly higher in patients than in controls. Loggia states that the PET signal increases were so consistent across participants, that it was possible to spot which were the patients and which were the controls simply by looking at the individual images prior to detailed statistical analysis of the data.
The release states that an additional finding indicated that among patient participants who had been asked to report their current levels of pain during the imaging session, those with the highest level of TSPO had reported lower levels of pain.
While upregulation of TSPO is a marker of glial activation, an inflammatory state, animal studies have suggested that the protein can actually limit the magnitude of glial response after its initiation and promotes the return to a pain-free, pre-injury status, Loggia says.
“This means that what we are imaging may be the process of glial cells trying to ‘calm down’ after being activated by the pain. Those participants with less pain-related upregulation of TSPO may have a more exaggerated neuroinflammatory response that ultimately leads to more inflammation and pain. While larger studies would be needed to further support this interpretation, this evidence suggests that drugs called TSPO agonists, which intensify the action of TSPO, may benefit pain patients by helping to limit glial activation,” Loggia notes.
[Source(s): Medical News Today, Massachusetts General Hospital]
