New research suggests that a group of drugs being developed to treat patients with mood disorders could also relieve chronic pain.
Published in Science Translational Medicine, the report outlines how inhibiting FKBP51, a protein that shapes the body’s response to stress, can block pain from injury without affecting normal pain response. Scientists believe this new finding offers new targets for future pain medications.
Researchers from the University College London (UCL) studied genetically modified mice that lacked this particular protein. Variations in the human FKBP5 gene are linked to an increased risk of individuals developing stress-related psychiatric disorders. These include major depression and post-traumatic stress disorder (PTSD).
After examining the mice, the scientists discovered that mice without FKBP51 experienced reduced chronic pain from nerve damage and arthritic joints.
The researchers then tested a KBP51-blocking compound called SAFit2. The administration of the specific FKBP51 inhibitor SAFit2 “reduced the severity of an established pain state, confirming the crucial role of spinal FKBP51 in nociceptive processing.”
“The compound was designed to have positive effects on mental health, but we have discovered that it also has significant benefits for physical pain syndromes,” Dr. Sandrine Géranton, PhD, Sobell Department of Motor Neuroscience and Movement Disorders at UCL Institute of Neurology, London, said in a news release. “Who wouldn’t want a treatment that relieves chronic pain while also making you less stressed? This was an experimental study with mice, but if this could be successfully translated into a treatment for patients, it would be a win-win.”
The scientists also found that an injury can trigger long-term epigenetic changes in spinal cord sensory circuits, which can lead to an increased production of FKBP51.
Research was funded by the Medical Research Council based in the United Kingdom.
Maiaru M, Tochiki K, Cox M et al. The stress regulator FKBP51 drives chronic pain by modulating spinal glucocorticoid signaling. Sci. Transl. Med. 2016; 8(325):325ra19-325ra19. doi:10.1126/scitranslmed.aab3376.
This article originally appeared on Clinical Pain Advisor