Future Directions of NMOSD Research: Brian G. Weinshenker, MD

"Patients with neuromyelitis optica just don’t randomly develop this disease. They [have] these central checkpoint defects that allow them to develop these auto- and poly-reactive cells which presumably makes them prone to all kinds of autoimmunity, including AQP4-IgG."

There’s no debate that the overall knowledge of and care for patients with neuromyelitis optica spectrum disorder (NMOSD) has drastically improved over the last several years. Once not even considered an independent disease, researchers have uncovered more about the presentation and diagnosis of NMOSD and how it differentiates from other demyelinating diseases such as multiple sclerosis.

A distinguishable feature for patients with NMOSD is that they will often encounter a variety of other autoimmune disorders and complications. Aquaporin-4 (AQP4), the target antigen of NMO-IgG, is a water channel protein highly concentrated in the spinal cord gray matter that has been widely recognized for playing a direct role in the pathogenesis of NMOSD. This finding has led to more homogenous populations for clinical trials and targeted FDA-approved treatments, which have entered the fold in just the past 2 years.

Despite these advancements, there remains several questions surrounding disease progression and treatment optimization, according to Brian G. Weinshenker, MD, a professor of neurology at Mayo Clinic College of Medicine. In an interview with NeurologyLive, Weinshenkerdiscussed areas within the NMOSD space that have improved and others that need continued research.