Neurology

Mouse studies suggest inhibiting signaling between RTN4R, RTN4RL2 and their ligands could help treat white matter stroke. In a mouse model of the disease, white matter levels of three negative regulators of Nogo signaling were lower and the number of oligodendrocyte progenitor cells (OPCs) differentiating into astrocytes were higher than in normal mice. In a young adult mouse model of white matter stroke, a chimeric RTN4R-RTN4RL2-Fc fusion protein that inhibits the Nogo signaling ligands MAG, OMG and RTN4 increased differentiation of OPCs into oligodendrocytes compared with a control IgG-Fc fusion protein. In an aged mouse model of white matter stroke, the ligand inhibitor increased forelimb motor control. Next steps include identifying additional signaling pathways that affect the differentiation of OPCs in white matter stroke.

GlaxoSmithKline plc has GSK249320, a mAb against MAG, in Phase II testing for cerebral stroke...