Their study, “Serum [Met5]-enkephalin levels are reduced in multiple sclerosis and restored by low-dose naltrexone,” appeared in the journal Experimental Biology and Medicine.
MS, an autoimmune disease that affects the nervous system, develops due to a disruption in communication between the brain and the body. Doctors often prescribe low-dose naltrexone (LDN) off-label for a variety of autoimmune diseases, including MS. Naltrexone helps make MS more tolerable by blocking opioid receptors that regulate pain, reward and addictive behaviors. This causes OGF levels to rise.
Studies show that treating MS patients with LDN improves their quality of life and reduces fatigue. But scientists have not figured out how LDN works in MS.
To find out, Penn State researchers examined serum OGF levels in MS patients and MS mouse models. They determined that MS patients have significantly lower OGF levels than do healthy people. Also, mouse models of MS have shown that decreases in OGF levels predicted MS disease development, and that treating MS-afflicted mice with LDN appeared to restore their OGF levels while having no effect on OGF levels in regular mice.
The study demonstrates that OGF — also known as [Met5]-enkephalin — is lower in MS patients than in healthy people. It also supports the practice of measuring OGF levels in MS patients as a noninvasive biomarker.
“Identification of OGF as a potential biomarker for MS supports our hypothesis for many years that the OGF signaling is dysregulated in MS patients,” Dr. Patricia McLaughlin, professor of neural and behavioral sciences at Penn State University College of Medicine, said in a press release.
“Randomized, controlled clinical trials on the treatment of MS patients with LDN are warranted given these new observations that OGF levels are deficient in these patients and restored following therapy,” she added. “Further research on potential biomarkers associated with this pathway is needed in order to establish early detection of MS, and possibly understand the etiology of MS.”
Dr. Steven R. Goodman, editor-in-chief of Experimental Biology & Medicine, said McLaughlin and her colleagues “have researched the OGF-OGF receptor (OGFr) regulatory axis for several decades, and this seminal discovery of dysregulation in OGF expression in MS patients, and animal models, is very exciting and could lead to prognostic biomarkers for this autoimmune disorder.”