Blocking a molecule that is overly abundant in the nervous system of multiple sclerosis (MS) patients, and has been linked to nerve cell damage in animals, worked to significantly ease inflammation, demyelination, and neurodegeneration in mouse models of secondary progressive MS (SPMS), a study reports.
Treatment to inhibit this molecule also helped the SPMS mice recover damaged neural networks and motor ability.
The study “Inhibiting repulsive guidance molecule-a suppresses secondary progression in mouse models of multiple sclerosis” was published in the journal Cell Death & Disease.
Earlier research demonstrated that repulsive guidance molecule-a (RGMa) is overabundant in the central nervous system of MS patients. This molecule is expressed at the cell membrane and is critical for the formation of neural networks, but it also works to inhibit nerve fiber (axon) growth and affects immune regulation.
Studies done in mouse models of MS showed that RGMa contributes to the progression of MS-like disease, promoting inflammation and nerve cell death. Importantly, treating these animal models with an antibody that blocks RGMa was seen to ease disease manifestations.
Based on this knowledge, a team of researchers at Osaka University, in Japan, wondered if this treatment would also confer benefits in mouse models of SPMS.
The researchers used a mouse model of SPMS — the non-obese diabetic mice with experimental autoimmune encephalomyelitis, the NOD-EAE model “that closely resembles SPMS,” they noted.
Mice were divided into three groups: two treated intravenously with a humanized antibody targeting RGMa at two different doses, and one given a related antibody with no therapeutic effect to serve as controls.
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