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Risk for post-injury spine damage increases with age
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Immune cells in the central nervous system of elderly mice failed to activate an important signaling pathway, lowering the chances of repairing the spine after an injury, according to recent study findings.
In younger adult mice, microglia — the central nervous system immune cells called into action by spinal cord trauma — activate the interleukin-4 alpha receptor, which then recognizes and makes use of an inflammation-related signaling chemical; however, the microglia in elderly mice do not have this affect at all.
“The microglia are regulated by several different cell types and different signals, and it appears a lot of those systems change with age,” Jonathan P. Godbout, PhD, an associate professor of neuroscience at The Ohio State University and senior author of the study, said in a press release about the study. “We’ve shown evidence that this more severe injury occurs in an aging animal, and that the difference in recovery is related to the ability to express the receptor. The consequence is we have a different profile of cells at the injury site, and in aging mice, that environment is less reparative.”
According to the researchers, lesions on the injured spinal cords of elderly mice were an average of 38% longer than in the younger mice. Furthermore, the elderly mice continued to have hindered mobility in their hind legs, whereas the younger mice regained all movement.
“Though any therapy based on this research would take many years to develop, Godbout … said that finding a drug that could stimulate expression of the IL-4 alpha receptor in elderly spinal cord patients might have potential to improve their outcomes,” the release concluded.
Disclosure: The study was supported by the National Institute on Aging, a Med into Grad Fellowship from the Howard Hughes Medical Institute and an Ohio State Presidential Fellowship.