When the fatty sheaths that insulate nerve fibers in the brain become damaged, the result is multiple sclerosis (MS). But the cause of this destruction has long baffled researchers. One group now reports that a protein called syncytin might be at fault.
Christopher Power of the University of Calgary in Alberta and his colleagues report in the October Nature Neuroscience that brain tissue collected from MS patients at autopsies harbors about three times as much syncytin as does postmortem brain tissue from people without MS.
To see what role syncytin might play in MS, the researchers cultured human brain cells in lab dishes. Using a genetically engineered virus that promotes syncytin production, the scientists induced cells called astrocytes to crank out the protein. The cells then released inflammatory proteins and damaging oxidizing compounds called free radicals. This combination killed oligodendrocytes, brain cells that maintain the myelin sheaths that insulate nerve fibers.
When the scientists injected the syncytin-promoting virus into the brains of live mice, the viruses invaded astrocytes and caused these cells to produce large amounts of the protein. Within 2 weeks, the mice developed muscle-coordination problems reminiscent of MS symptoms. Mice given an antioxidant recovered.
The gene for syncytin is an oddity. Scientists hypothesize that it was captured from retroviruses that invaded the human genome roughly 1 million years ago (SN: 5/13/00, p. 318: Available to subscribers at Placental Puzzle). The gene is normally quiescent, except when playing a role in placental development, says Mark P. Mattson, a neuroscientist at the National Institute of Aging in Baltimore.
“It’s not clear why the gene for syncytin is activated in astrocytes of MS patients,” he says. Even so, the finding could open up a new strategy for developing treatments for MS.