For decades, scientists’ quest to discover the cause of Alzheimer’s disease has remained as elusive as its treatment. Many studies have suggested a role for various pathogens—a bacterium or virus—that may jumpstart the process that leads to the disease. But after hundreds of analyses, no concrete associations or plausible mechanisms between bacterial or viral pathogens had emerged.

But now: Researchers have made a major step forward.

In the search for answers, scientists had already established that sticky clumps of plaques known as beta-amyloid in the brain are a hallmark of Alzheimer’s disease. Yet the unanswered question remained—why do some people develop those bits of plaque and others do not? Solving this mystery has long been considered the holy grail in developing prevention strategies to spare millions of adults the ravages of Alzheimer’s.

To address this question, researchers at the Icahn School of Medicine at Mount Sinai in New York City examined more than 600 samples of brain tissue from deceased donors both with and without Alzheimer’s disease. One of the goals was to find evidence of viral strains within the brain tissue samples. Along with that, the researchers analyzed the influence of various viruses on genes and proteins that are involved in the development of Alzheimer’s disease.

Study results: Human herpes virus strains 6A and 7, which cause the common childhood illness roseola (characterized by high fever and a rash), were found in levels nearly twice as high in the brains of people with Alzheimer’s disease than in those without the brain disorder. Like many other viruses, after the acute infection during childhood, this virus remains dormant in the body. These findings were then confirmed with additional donated brain tissue from other research organizations.

Bottom line: The viruses are not suspected to cause Alzheimer’s disease, but the researchers suggest that somehow herpes virus strains 6A and 7 may promote an immune response that leads to the deposits of beta-amyloid plaque in the brain.

“This is the most compelling evidence ever presented that points to a viral contribution to the cause or progression of Alzheimer’s,” said one of the study’s authors, Samuel E. Gandy, MD, PhD, professor of neurology and psychiatry and director of the Center for Cognitive Health and NFL Neurological Care at Mount Sinai.

This study suggests that certain viruses may play a role in the Alzheimer’s process. It’s too early to know what these findings mean in terms of prevention or treatment. But further research will likely lead to better understanding and then major steps forward.