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Alzheimer’s protein could help MSamyloid-beta may thwart attack on central nervous system

By Laura Sanders

A much-maligned molecule that is devastating in the brain may have therapeutic potential outside it. The amyloid-beta protein, which piles up in the brains of people with Alzheimer’s disease, reverses paralysis in mice with symptoms of multiple sclerosis.

The unexpected finding, published in the Aug. 1 Science Translational Medicine, could mean that A-beta or molecules like it may one day form the basis of a treatment for multiple sclero-sis in people.

In MS, rogue immune cells penetrate the brain and spinal cord and attack myelin, a substance that is necessary to keep nerve cell signals moving at full speed. Damage and inflammation from this attack can leave a person with paral-ysis, numbness, vision problems and extreme fatigue.

A-beta is found in the brains of peo-ple with MS, but scientists do not know precisely what effect it has there, if any.

To investigate that question, Lawrence Steinman of Stanford University and colleagues tried injecting A-beta into mice’s abdomens, thinking it would worsen symptoms. “We expected that either nothing would hap-pen or the disease would worsen because this is an infamous, villainous mol-ecule,” he says.

Instead, the mice got better. In several different kinds of mice designed to have symptoms similar to the human disease, A-beta injections into the body reduced paralysis and low-ered brain inflammation. “The outcome was unmis-takable,” Steinman says.

To do its good work, A-beta didn’t need to enter the brain, the research-ers think. After the experiments, there was no evidence of the molecule piling up there. Instead, A-beta exerted its protective effects in the rest of the body,

perhaps by calming down immune cells circulating in the blood and preventing them from waging war on the brain.

The data look convincing, but it’s not clear exactly how A-beta works to ease multiple sclerosis symptoms, says biochemist Charles Glabe of the University of California, Irvine. More studies are needed to clarify how A-beta

interacts with the immune system, he says.

Other proteins similar to A-beta in shape may bring the same benefit, and with-out the potential dangers associated with A-beta. Steinman and his col-leagues are currently test-ing candidates.

Much more work needs to happen before such a treatment could be devel-oped for use in people. “For these approaches, we

have to learn what the drawbacks are,” Steinman says. Dampening the immune system could heighten the risk of brain infection, for instance. And there’s always a possibility that the results in mice won’t hold up in humans. s

“We expected that either

nothing would happen or

the disease would worsen because this

is an infamous, villainous molecule.”

LAwrence SteinMAn

Body & Brain for more Body & Brain stories, visit www.sciencenews.org

In a healthy gut, a thin layer of mucus-lined intestinal wall separates billions of beneficial bacteria from the immune sys-tem. But in the throes of an intestinal infection, the walls are breached and both infectious and beneficial microbes (green) penetrate the intestinal wall (blue). Immunologist timothy hand of the national Institute of allergy and Infectious diseases in Bethesda, Md., and his colleagues show online august 23 in Science that in mice these breaches cause immune cells to lose their tolerance for the beneficial bacteria. the immune system’s t cells form long-lasting memory cells that harbor the ability to bring the beneficial bacteria under friendly fire in subsequent encounters. the new findings suggest a role for mis directed t cells in inflammatory bowel ailments such as crohn’s disease, in which there is evidence of barrier breaching and t cell dysfunction. In this way, gut infections might prime t cells for a subsequent destructive role and, hand suggests, predispose some people to the diseases. — Nathan Seppa

Microbe misunderstanding

14 | science news | september 22, 2012 www.sciencenews.org

body_brain.indd 14 9/5/12 12:48 PM