Abstract
Multiple sclerosis (MS) is a chronic immunological disorder of multifactorial etiology. Genetics, geographical location, age, and gender are risk factors, but the underlying causes are not fully defined. Research has provided substantial evidence that pro- and anti-inflammatory cytokines, as well as glial cell proliferation are involved in the progression of the disease. However, there is still a need to define noninvasive biomarkers to track the onset and course of MS. New treatments are effective at reducing signs and symptoms of the disease, but little change has been made in altering the overall course of MS.
Clinical reports from individuals using a low dose of the opioid receptor antagonist naltrexone prompted research using animal models of chronic experimental autoimmune encephalomyelitis (EAE) or relapsing-remitting EAE (RR-EAE). These studies reported that serum levels of the endogenous peptide Opioid Growth Factor (OGF), chemically termed [Met5]-enkephalin, declined during the course of disease and could be restored to normal following therapeutic intervention. β-endorphin, another endogenous neuropeptide, was less responsive to treatment, suggesting that OGF may be a selective biomarker for MS that can be obtained non-invasively in order to monitor the course of disease.
There is a rapid decrease in OGF serum levels within days of EAE induction, as well as reduced levels of OGF in individuals with MS. This reduction in the negative growth factor may contribute to the uncontrollable lymphocytic proliferation and cytokine storm observed in early stages of MS that correspond to the physical and mental decline measured in humans, and to the behavioral deficits and central nervous system pathology recorded in animal models. Therapies that increase OGF serum values and result in improved clinical signs and perceived good health are warranted.
Keywords
Opioid Growth Factor, [Met5]-enkephalin, ELISA tests, MS, Experimental autoimmune encephalomyelitis