A therapeutic target for the treatment of acute spinal cord injury (SCI) may have been identified, according to a news release from the Universitat Autònoma de Barcelona (UAB).
Researchers note in a new study published in the Journal of Neuroscience that giving mice a drug that prevents loss of myelin—the insulating sheath around nerve fibers that allows signals to be transmitted—increases the mice’s mobility after SCI, per the release.
According to the release, an international team of scientists coordinated by Rubèn López Vales, of the Department of Cell Biology, Physiology and Immunology of the UAB, the UAB Institute of Neuroscience, and the Centre for Networked Biomedical Research in Neurodegenerative Diseases (CIBERNED), has discovered that lysophosphatidic acid plays a major role in degenerative processes in spinal cord injuries.
Lysophosphatidic acid is a lipid that acts as a signaling molecule between the different cells in the organism, thus controlling many biological functions. The researchers observed that, following an SCI, levels of this lipid rise significantly in the nerve tissue and there is a loss of myelin, the electrically insulating material that surrounds nerve fibers and is needed for the transmission of nerve signals, the release explains.
The scientists also identified the biological receptor, known as LPA1, through which this lipid multiplies the harmful effects of an SCI. In experiments with mice, the use of a drug that prevents the interaction of lysophosphatidic acid with LPA1 led to a drastic reduction in myelin loss, and the mice’s locomotor performance improved after the spinal cord injury, per the release.
Following spinal cord injury, mice displayed only occasional, uncoordinated locomotion, but 87% of those treated with the drug displayed normal, coordinated locomotion. In addition, only 10% of the untreated mice could run at 20 cm/s and none at 25 cm/s while, on applying the drug, 50% could run at 20 cm/s, 40% at 25 cm/s, and 30% at 30 cm/s, the release states.
Researcher Rubén López says, in the release, that, “this discovery could also open the door to treatments for other neurodegenerative illnesses in which myelin loss plays a major role, such as multiple sclerosis.”
[Source(s): Universitat Autònoma de Barcelona; Science Daily]
