AGING
August 14, 2012

What Alzheimer's Tells Us about Multiple Sclerosis

The culprit in Alzheimer's disease, amyloid-beta, might prevent multiple sclerosis. Come again?

Amyloid-beta, the substance that accumulates in the aging brain and forms the plaques in Alzheimer’s disease, may actually reduce or prevent the symptoms of another neurodegenerative disease, multiple sclerosis (MS).

In multiple sclerosis, the cells of the immune system attack myelin, the insulating tissue of the central nervous system, which speeds communication between cells. It’s too soon to tell whether or how the finding might lead to a new treatment for MS, but the early results do tell us a bit about how the diseases work.

Instead of exacerbating symptoms as they had expected, the amyloid-beta injections actually reduced or prevented the onset of symptoms.

Researchers have long known that amyloid-beta and its precursor protein are found in MS lesions in the central nervous system. So finding that an injection of amyloid-beta into the bodies of mice could actually reduce symptoms of MS came as a bit of a surprise to the researchers who crafted the study.

The team at Stanford University, led by Lawrence Steinman, wanted to see what would happen if amyloid-beta were injected not into the nervous systems of mice who were engineered to develop an MS-like disease, but into their bodies. They found that instead of exacerbating symptoms, the injections actually reduced or prevented the onset of symptoms.

"We figured it would make it worse," Steinman said in a news release. But it didn’t – it made it better. Understandably surprised at the findings, the team repeated the experiment, and found the same results the second time around.

To look further into the mechanism, the team took immune cells from mice who had received the amyloid-beta injections and injected them into another group of mice, also destined to develop MS. In this second group of mice, after receiving the immune cells of their counterparts, symptoms like motor decline and paralysis were again delayed or prevented. These mice also had reduced levels of the inflammation that is typical of MS flare-ups.

Further investigation also found that when mice lacked the gene for amyloid-beta, they developed much worse symptoms of MS and died more frequently, suggesting that indeed amyloid-beta has a protective effect – at least under some circumstances.

What do these findings all mean? “There probably is a multiple-sclerosis drug in all this somewhere down the line,” said Steinman. In other words, it’s not clear how exactly this new research will change the game – either for MS or for Alzheimer’s – but it does underline how a single compound can be destructive in one scenario and protective in another. We’ll be interested to see what developments – and surprises – the next research brings.

The study was published in the journal Science Translational Medicine.

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