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The proteins were traditionally thought to be garbage that accumulates in the brain with age. But Moir noticed that they looked a lot like proteins of the innate immune system, a primitive system that is the body’s first line of defence against infections.

Elsewhere in the body, such proteins trap microbes — viruses, fungi, yeast and bacteria. Then white blood cells come by and clear up the mess. Perhaps amyloid was part of this system, Moir thought.

He began collaborating with Rudolph E. Tanzi, also at Harvard Medical School and Massachusetts General Hospital, in a study funded by the National Institutes of Health and the Cure Alzheimer’s Fund. The idea was to see if amyloid trapped microbes in living animals and if mice without amyloid proteins were quickly ravaged by infections that amyloid could have stopped.

The answers, they reported, were yes and yes.

In one study, the group injected Salmonella bacteria into the brains of young mice that did not have plaques.

“Overnight, the bacteria seeded plaques,” Tanzi said. “The hippocampus was full of plaques, and each plaque had a single bacterium at its center.”

In contrast, mice that did not make beta amyloid succumbed more quickly to the bacterial infection, and did not make plaques.

For years, researchers had been fixated on the idea of plaques as a sort of trash that accumulated in the brain, so few had asked if there might be some other explanation.

As Dr. Samuel E. Gandy, a professor of neurology and psychiatry at the Icahn School of Medicine at Mount Sinai Hospital in New York, explained, there was a long and persuasive body of research laying out the Alzheimer’s pathway: Plaques form and set off the formation of tangled threadlike tau proteins. Then, as tangles of tau kill nerve cells, the brain becomes inflamed, resulting in the killing of many more nerve cells.