The hallmark degenerative process in spinal cord injury may be caused by lysophosphatidic acid, the lipid that acts as a signal between various cells, according to findings published in The Journal of Neuroscience.
The hallmark degenerative process in spinal cord injury may be caused by lysophosphatidic acid, the lipid that acts as a signal between various cells, according to findings published in The Journal of Neuroscience. The researchers also determined that locomotive function was improved after drug treatment in animal models, while demyelination was reduced.
Researchers from the Universitat Autonoma de Barcelona (UAB) in Spain used models of normal spinal cord to determine the potential contribution of lysophosphatidic acid in degeneration of the spinal cord. The researchers injected lysophosphatidic acid into normal spinal cord and determined that lysophosphatidic acid induces microglia and macrophage activation as well as demyelination.
The authors noted that while lysophosphatidic acid had been identified in the central nervous system, including neural progenitor cell physiology, astrocyte and microglia activation, neuronal cell death, axonal retraction, and development of neuropathic pain. But the researchers also said that the involvement of lysophosphatidic acid in the central nervous system pathology had not yet been fully analyzed.
“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,” explained UAB researchers Ruben Lopez in a press release. The researchers believe in the future, new therapeutic targets may be able to treat acute spinal cord injuries, which currently have no clinically effective treatment.
Additionally, the scientists identified the biological receptor LPA1 in this investigation. LPA1 is the mechanism through which the lipid multiples the harmful effects of a spinal cord injury, the authors explained. Using mice models, the researchers discovered that the drug that prevents lysophosphatidic acid from interacting with LPA1 allowed for significant reduction in demyelination.
The animal models’ locomotive performances improved after the spinal cord injury, too. After the spinal cord injury, the mice sometimes displayed uncoordinated locomotive function. However, nearly all of the mice (87 percent) of those treated with the drug displayed normal locomotive function. Plus, the researchers said, just 10 percent of the untreated mice were able to run at speeds of 20 centimeters per second (cm/ s) and none were able to reach 25 cm/ s. After applying the drug, half of the mice could run at speeds of 20 cm/ s, 40 percent reached 25 cm/ s, and 30 percent ran at 30 cm/ s.