AsianScientist (Jan. 31, 2018) – In a study published in the journal Scientific Reports, a team of scientists at Osaka University, Japan, have discovered an antibody that may be used in the treatment of Devic’s disease.
Devic’s disease, also known as neuromyelitis optica (NMO), is a central nervous system disorder that primarily affects the eye nerves (optic neuritis) and the spinal cord (myelitis). It occurs when the body’s immune system produces autoantibodies in the central nervous system.
Autoantibodies are proteins that target one or more of the individual’s own proteins. Most patients with NMO present severe clinical symptoms, such as blindness in one or both eyes, weakness or paralysis in the legs or arms, and painful spasms. At present, there is no cure for NMO, and no medications have been specifically approved to treat it.
In this study, the researchers led by Dr. Kana Harada at Osaka University identified an antibody that alleviates the symptoms of NMO. The team started off by developing a rat model that mimics the pathology of intractable NMO by injecting NMO-immunoglobulin G (IgG) antibodies into the spinal cord.
In contrast to previous animal models of NMO that generally produced disseminated lesions, the new localized model has a single well-demarcated inflammatory lesion, allowing precise investigation of the correlation between the lesion and the deficit in motor function of the corticospinal tract.
The researchers then treated the rats with an antibody against a molecule called protein repulsive guidance molecule-a (RGMa), which has been implicated in other autoimmune-related neurodegenerative disease.
“Recently, a role for (RGMa) in the immune system has become apparent. Inhibiting RGMa with its antibody in multiple sclerosis in rats promotes motor recovery after spinal cord injury and improves disease scores,” said Harada. “Because NMO and multiple sclerosis are both immune-mediated neurodegenerative diseases with broadly comparable symptoms, we hypothesized that anti-RGMa antibody may have a suppressive effect on NMO.”
They found that the anti-RGMa antibody preserved astrocytes, a type of cell in the central nervous system, also reducing inflammatory cell infiltration and damage to the neurons of rats. Moreover, the onset and severity of clinical symptoms such as hind limb paralysis was delayed by the treatment.
“In rats that developed optic neuritis, relaxation of neurological symptoms was observed by suppressing RGMa using humanized monoclonal anti-RGMa antibody antibodies,” said corresponding author Dr. Yuki Fujita of Osaka University. “Also, the inhibition of RGMa promotes restoration of injured neural networks, presumably leading to a delay in the progression of the secondary phase of NMO.”
These findings support the potential of humanized anti-RGMa antibody as a valid therapeutic approach against NMO, the authors said.
The article can be found at: Harada et al. (2018) Inhibition of RGMa Alleviates Symptoms in a Rat Model of Neuromyelitis Optica.
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Source: Osaka University; Photo: Shutterstock.
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