The virus theory is far from being accepted by most Alzheimer’s experts. Some raise the chicken-or-egg question: Could viruses found in greater amounts in Alzheimer’s brains be consequences of the disease or even, as Dr. Lennart Mucke, director of the Gladstone Institute of Neurological Disease in San Francisco said, “innocent bystanders”?

Dr. Mucke called the new study “impressive and very well designed.” But, he noted, “there have been many speculations and even outright claims that infections contribute to the development of Alzheimer’s disease.”

“None of them has held up after rigorous cause-effect evaluations,” he added.

Still, the new findings will be bolstered by another upcoming study in Neuron, led by Rudolph Tanzi and Robert Moir, neuroscientists at Massachusetts General Hospital and Harvard, who have broken ground on the virus idea for years.

Their new experiments, performed in mice and three-dimensional brain cells in a dish, found that the same herpes species ignited a protective reaction in amyloid, a protein present in all human brains. Dr. Tanzi describes this as “seeding” the amyloid, causing it to ensnare the virus in fibrous nets that form plaques.

In this way, he said, viruses and other microbes are the “prequel” to the prevailing theory that Alzheimer’s is caused by amyloid accumulation the brain cannot clear out.

For the study published Thursday, Dr. Dudley, who described himself as a “big data guy,” not an Alzheimer’s expert, was asked by the National Institutes of Health to help generate new Alzheimer’s ideas by analyzing information from a consortium involving many brain banks and researchers.

Dr. Dudley was interested in whether existing drugs could be repurposed to treat Alzheimer’s, which has so far resisted all drugs tested in hundreds of clinical trials. To start, he and colleagues created computer models mapping the molecular and genetic networks disrupted as Alzheimer’s progresses.