Guzman-Soto and colleagues (2016) noted that recent findings have shown that GnRH administration in an animal model of multiple sclerosis (experimental autoimmune encephalomyelitis, EAE) improves clinical signs of locomotion. These researchers examined if the administration of the synthetic analog of GnRH, leuprolide acetate (LA) -- besides its effects on clinical signs of locomotion -- also has an effect on the activation/expression levels of molecular markers of EAE, namely transcription nuclear factor (NF)-κB and the pro-inflammatory cytokines IL-1β, IL-17A, IL-23 and TNF-α. EAE spinal cords were collected from control and LA-administered rats. Lumbar sections were processed at 4 different time points during the course of the disease to analyze NF-κB activation by chemiluminescent Western blot, and during the EAE recovery phase to evaluate pro-inflammatory cytokine levels by quantitative real-time PCR. It was found that LA administration to EAE rats promoted a significant reduction of NF-κB activation during the course of the disease and also decreased the mRNA expression levels of the pro-inflammatory cytokines IL-1β, IL-17A and TNF-α in the EAE recovery phase; both effects were consistent with the decrease in the severity of clinical signs of locomotion induced by the treatment. The authors concluded that LA caused a reduction in the severity of locomotor activity, as well as in the activation of NF-κB and the number of pro-inflammatory markers in rats with EAE. They stated that these findings suggested the use of this agonist as a potential therapeutic approach for multiple sclerosis.