By Karen Weintraub
A protein thought to be a hallmark of Alzheimer’s may turn out to be helpful against multiple sclerosis, new research from Stanford University suggests.
Beta-amyloid has long been considered a prime culprit behind the brain degeneration of Alzheimer’s. But Stanford Neurology Professor Lawrence Steinman said he kept finding it and its precursor protein in the brains of MS patients. “The question is, what is it doing there? Certainly, MS doesn’t look like Alzheimer’s,” he said.
So he investigated the role of the protein in a mouse model of MS that’s close, but not exactly like the human version. He expected to see that the villain of Alzheimer’s was similarly destructive in MS, or at least had no effect at all.
Instead, he found that when he added beta-amyloid to the brains of afflicted mice, they got better – in many cases substantially so. “We tried three or four variations of the model to make sure it wasn’t a fluke,” he said. But it wasn’t. Giving sick mice beta-amyloid “makes the animals get better and it makes them get better quickly and quite noticeably.”
It’s much easier to help mice than people, though, Steinman said, warning that it’s too early to know whether people with MS will see the same benefit. MS is an autoimmune disease in which the body attacks the coating around white brain cells that speeds up brain messages. People with MS often complain of fatigue, dizziness, numbness and double-vision.
Steinman said additional research, not included in the new Science Translational Medicine study, suggests that the whole class of amyloid proteins – not just beta-amyloid – might be protective against the damage of MS. That class includes insulin, famous for its connection to diabetes, as well as the protein that causes Huntington’s disease.
“It’s very surprising because my education and my teaching has always been that beta-amyloid and probably other amyloid proteins are really bad for you,” said Steinman, who has launched a company to explore commercializing, alpha-crystallin, a safer amyloid protein for the treatment of MS.
So, if amyloids aren’t always the bad guys, what does that mean for Alzheimer’s?
Steinman said it’s too soon to tell. But it does raise questions about the so-called amyloid hypothesis of Alzheimer’s. Drugs based on that hypothesis are in clinical trials right now in patients. Pfizer announced last week that its trial of one of these drugs had failed to prevent Alzheimer’s in people with a high genetic likelihood of developing the disease.
It could be, as most scientists suspect, that the drug failed because it was not given early enough, before beta-amyloid worked irreversible damage on the brain. “But there are other possibilities,” Steinman said. “One is that the most wonderful theories with the strongest foundations are sometimes not completely right.”
Karen Weintraub, a Cambridge-based health/science journalist, is a frequent contributor to CommonHealth.