Chronic pain affects millions of people worldwide, yet popular treatments for pain — including surgery and opioid medications — can have disastrous side effects of their own. But with $1.8 million in funding from the National Institute of Neurological Disorders and Stroke (NINDS), a University of New England researcher will explore non-opioid treatments for chronic pain at the cellular level.
Benjamin Harrison, BSc, PhD, assistant professor of biochemistry and nutrition, will use the five-year R01 grant from the National Institutes of Health to study how to reduce the excitability of nociceptors, which are neurons that transmit pain signals in response to painful injuries.
Harrison and his team have discovered that nociceptors contain a protein called “CELF4,” an RNA binding protein they theorize inhibits the production of “pro-nociceptive,” or pro-pain-sensing, cellular components. Harrison’s research will focus on delivering CELF4 into pain neurons, where this protein will limit the synthesis of ion-channels, receptors, and other molecules that sensitize them.
Specifically, the researchers will study if a locally administered adeno-associated virus can stimulate production of CELF4 and reduce pain in those areas — an approach known as gene vector therapy.
Harrison remarked that the innovative approach could prove beneficial for those living with chronic pain but who do not want to undergo surgeries — which can be expensive and leave people with no sensation at all — or use powerful pain-reducing medications like addictive opioids.
“There are some chronic pain conditions that are simply intolerable, and people with those conditions are willing to do severe surgeries to reduce their pain,” Harrison remarked. “Using this novel gene therapy vector approach, we can develop pain therapies that are less invasive than surgery and carry fewer risks than conventional opioid medications.”
Future directions for the research could include partnerships with clinicians for clinical trials, Harrison said.
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