Could it be that Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection? New research by a team of investigators at Harvard leads to this startling hypothesis. This may explain the origins of plaque that pockmark the brains of people with Alzheimer’s.
It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease.
Published Wednesday in the journal Science Translational Medicine, supports the idea that a virus, fungus or bacterium gets into the brain, passing through the blood-brain barrier that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s.
So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans—and funding—are in place to start those studies.
For years, researchers had been fixated on the idea of plaques as a sort of trash that gathered in the brain. Few had asked if there might be some other explanation.
Recent data suggests that the incidence of dementia is decreasing. It could be because of better control of blood pressure and cholesterol levels, staving off ministrokes that can cause dementia. But could a decline in infections also play a role?
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Kumar D, Kumar V, Choi SH, et al. Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease. Science Translational Medicine 25 May 2016:340; 340ra72.