Karen Weintraub, Special for USA TODAY , KARE 8:07 AM. CDT May 27, 2016
Researchers at Harvard this week offered a new theory of Alzheimer’s disease that – if true – would upend our understanding of the disease and suggest new routes for treatment and prevention.
The researchers think that the immune system may play a key role in the development of Alzheimer’s, which slowly robs people of their memory and is eventually fatal.
A protein called beta amyloid, long considered the bad actor in Alzheimer’s, actually plays a positive role in fighting off bacteria and fungus in mice, worms and cells, the researchers showed in a new paper in Science Translational Medicine.
Assuming that’s also true in people, it suggests that getting rid of amyloid, as some drug trials have tried, could be dangerous, and approaches that stimulate the immune system could be safer and more effective.
In this view, Alzheimer’s would be triggered by a normal immune response gone astray or into over-drive in response to bacteria or other pathogens, according to the paper’s authors, Rudy Tanzi and Robert Moir, both of Harvard Medical School and Massachusetts General Hospital.
Amyloid “lights the fire,” said Tanzi, whose work has been supported by a grant from the Cure Alzheimer’s Fund. “We think it’s meant to be beneficial, but it can turn against you and cause problems.”
That doesn’t mean Alzheimer’s is contagious, but that some people’s brains may over-react to or get overwhelmed by a variety of pathogens, including chlamydia, herpes and the bacteria that causes Lyme disease, Tanzi said. It’s possible that younger people’s brains can handle such issues, but some older ones can’t.
Alzheimer’s is believed to begin in late middle age, though the symptoms may not be evident until a decade or more later.
This view also adds weight to the idea that adequate exercise, high quality sleep, healthy diet and other lifestyle factors like treating gum disease can help prevent Alzheimer’s, said Tanzi, who co-wrote a book, Super Genes, with Deepak Chopra, laying out the ways that healthy living can help people avoid Alzheimer’s.
James Hendrix, director of global science initiatives with the Alzheimer’s Association, agreed that lifestyle factors could make a crucial difference. “If our brain is functioning properly and working the way it should, it will be able to fight off infection,” he said.
Vaccines or drugs that reduce inflammation might also be helpful, though the timing of such approaches will be key, said Gary Small, a professor of psychiatry and aging at UCLA’s Semel Institute. His own research has shown that healthy people who took anti-inflammatory drugs for 18 months had better brain function than those who took a placebo. But if they started the drugs after Alzheimer’s began developing, it could accelerate the disease. “There’s a tipping point,” he said, but no one yet knows where that is.
Several scientists praised the new paper Thursday and encouraged researchers to continue the study.
“I think it’s a very elegant theory,” said Ashley Bush, a professor of neuroscience at the University of Melbourne in Australia.
The work is far from conclusive, however, and the ideas in the paper are not entirely new, Bruce Kagan, a professor of clinical psychiatry at UCLA, said via e-mail. “We ‘cured’ Alzheimers in mice over a decade ago, but none of these drugs work in humans.”
Moir said he came up with this new theory when looking at an immune protein called LL-37 that acts like amyloid. In moderation, LL-37 is essential for keeping the brain healthy, but an excess of the protein has been linked to ailments from heart disease to rheumatoid arthritis.
Alzheimer’s researchers had always considered amyloid to be “junk,” involved only in destructive activities, but Moir said he thought amyloid must also have a positive role, because animals have had it for 400 million years.
In the mice, worms and cells the team tested, amyloid helped kill pathogens by surrounding them and caging them in. Such clumps of amyloid have long considered the hallmark of Alzheimer’s Disease.