That's according to preliminary lab tests done on mice. It's too soon to know if the same strategy will work in people. But if it does, it may lead to new MS treatments.
The researchers included Stanford University's Lawrence Steinman, MD, and Shalina Ousman, PhD. Steinman is a professor in Stanford's neurology and neurosciences department, where Ousman also works.
With colleagues from various other institutions, Steinman and Ousman studied CRYAB, which is found in the eye's lens.
Previous research has shown that when MS develops, CRYAB turns up in the brain. That's a problem -- but it also inspired an intriguing solution that may help tame MS.
In MS, the body's immune system attacks myelin, the fatty sheath that insulates nerves. As a result, nerves can't communicate as well as they normally would.
The new study focuses on mice with a brain condition similar to MS. Some of the mice were genetically unable to make CRYAB.
The scientists injected human CRYAB into those mice. That eased the mice's symptoms and even reversed paralysis caused by their disease.
How It Works
In their study, the scientists argue that when CRYAB first appears in the brain, it's a troublemaker.
"For some reason, the protein [CRYAB] gets turned on in the brain where it's not expected to be," Steinman says in a Stanford news release.
Because CRYAB isn't expected in the brain, the immune system attacks it. That spurs a cascade of inflammatory chemicals, making matters worse.
But adding more CRYAB to the brain has the opposite effect. Additional CRYAB calms brain inflammation, according to the researchers.
"Remarkably, addition of that very same stress protein, akin to restoring the brakes that were failing, returns control," they write, calling CRYAB a "critical tipping point" in the development of MS.
The study appears in the advance online edition of the journal Nature.