Stanford Multiple Sclerosis MS Researcher Lawrence Steinman

Multiple Sclerosis Paralysis Cure from Alzheimer’s Cause

Researchers at Stanford University note that a molecule that’s generally regarded as playing a major role in Alzheimer’s disease has a rather surprising effect on a different condition. Specifically, researchers have found that this notorious molecule has an unexpected reversal effect on the paralysis and inflammation in specific animals in which multiple sclerosis (MS) has been observed.

Over the years, A-beta, a peptide otherwise known as beta-amyloid, has been reviled by brain researchers for many reasons. The bit of protein has been identified as the primary ingredient of amyloid plaques, which builds up in the brains of those with Alzheimer’s disease, those who have suffered brain injuries, or anyone undergoing the normal aging process. According to research lead by senior author Lawrence Steinman, A-beta also appears in concentrations in MS lesions.

Science Translational Medicine recently reported on this discovery in an online feature, which followed disappointing news about the failure of a clinical trial geared toward slowing down the progression of Alzheimer’s disease. The trial was to eliminate the molecule, A-beta, from the bloodstream of Alzheimer’s patients, and, while the results may have been initially disappointing, the findings may shed light on the ways to successfully treat MS.

Multiple sclerosis is an inflammatory autoimmune disease that affects the brain and spinal cord. The disease occurs when immune cells infiltrate the nervous system–specifically the brain and spinal cord–and begin affecting the insulating coatings of nerve cells’ axons. When the protective coating of the axons is damaged, the cells do not transmit signals as they normally do, resulting in conditions such as blindness, loss of muscle control, as well as trouble with other normal activities such as attention and speech.

Multiple Sclerosis MS Demyelinization

A-beta has been observed to cause damage to many types of cells that have been isolated in lab dishes, and when administered directly to the brain, it has adverse, inflammatory effects. However, despite this basic knowledge, the exact physiological effects A-beta has on Alzheimer’s or MS patients remains shrouded in mystery, according to Steinman. Steinman and his associates surmised that if A-beta played a negative role with regard to Alzheimer’s (through myelin), then it more than likely played a dubious role in the nervous systems of patients with MS.

Using a mouse model that Steinman had employed while conducting previous work on the development of an MS drug, he began testing to see how a mouse’s autoimmune response would react to direct injections of A-beta into the belly rather than the brain. “We figured it would make it worse,” Steinman said. To his whole team’s surprise, the mice whose immune systems received A-beta administrations prior to the onset of the symptoms showed both lessened severity and even reversal of paralysis.

The team of researchers went on to conduct similar experiments using other mouse models. As with the previous experiment, they primed mice immune cells in such a way as to “train” them to attack myelin. This time around, the researchers collected the immune cells from the mice after about 10 days and injected them into a different set of mice who had not received any A-beta administrations. Steinman then observed the reactions of the new set of mice. They showed a response that was similar to the first set.

Results from the various mouse model tests showed not only that administering A-beta into the stomachs of mice increased the immune response related to MS, but also decreased paralysis, inflammation, and lesions in the brain and spinal cord. More importantly, it did all of that without increasing plaques in the brain. In other words, they didn’t give the mice Alzheimer’s by injecting them in the stomach with A-beta.

After seeing all of that, the research team wanted to see what would happen when they pushed A-beta levels down rather than up. Not only did these same MS-primed mouse models not get better, they developed extreme symptoms and died sooner and more often than normal mice who underwent the same regimen.

Consequently, researchers were able to conclude that the effect of the A-beta peptide on the immune system had nothing to do with the action on the brain itself, but instead had to do with the immune cells before they reached the brain. The protection A-beta provides in the mouse model of multiple sclerosis appears to be related to the immune suppressing effects in the body’s tissue rather than in the direct interaction with the brain.

“There probably is a multiple-sclerosis drug in all this somewhere down the line,” Steinman predicted.


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