Despite decades of research, scientists have made little progress in halting Alzheimer’s disease, a form of dementia. But researchers may have recently discovered a potential breakthrough. Pam Belluck at The New York Times reports that two new studies show a relationship between two types of herpes viruses and the development of Alzheimer’s.

The relationship was first found during a study commissioned by the National Institutes of Health. The research team created computer models that mapped the genes that were disrupted or activated during the progression of Alzheimer’s. They found that many of the genes that clicked on during Alzheimer’s are the same genes that activate when the body is fighting a virus.

Maggie Fox at NBC reports that researchers then looked at DNA and RNA sequences collected from 622 brains afflicted with Alzheimer’s and 322 disease-free brains, finding that two herpes viruses, HHV-6A and HHV-7, were more common in the brains of people who died of Alzheimer’s. People with more severe cases of the disease showed more signs of the viruses. Those herpes strains, which cause a mild childhood disease called roseola, are found in 90 percent of children in the United States and usually go dormant in childhood, but can reactivate in times of illness or stress. The research appears in the journal Neuron.

The study is by no means conclusive evidence that the viruses cause Alzheimer’s. But it is possible that the viruses worsen the disease's symptoms. As the disease progresses, the viruses may come out of dormancy, eliciting an immune reaction and leading to the formation of the brain plaques seen in Alzheimer’s patients. “These viruses are probably significant players in driving the immune system in Alzheimer’s,” Joel Dudley of the Icahn School of Medicine and senior author of the study, tells Belluck. “I think they’re like gas on the flames of some pathology that may be immune-driven.”

Leah Rosenbaum at ScienceNews reports that there is more recent support for this theory. In a second, unpublished study that will soon also appear in Neuron, researchers exposed mouse and brain cells to the implicated herpes viruses. The exposure led to a reaction in which protein fibers called amyloids, which cause the plaques found in Alzheimer’s patients' brains, were formed, perhaps to ensnare the viruses as part of immune response. The researchers propose that the activated viruses cause a buildup in amyloid plaques, which then triggers Alzheimer’s.

Despite these studies, Lennart Mucke, director of the Gladstone Institute of Neurological Disease in San Francisco, tells Belluck that, though the Dudley study is impressive, these herpes viruses could be unrelated to Alzheimer’s. Researchers have been down this road before. “[T]here have been many speculations and even outright claims that infections contribute to the development of Alzheimer’s disease,” he says. “None of them has held up after rigorous cause-effect evaluations.”

Whatever the case, the new studies make the once-controversial idea that a virus is involved in Alzheimer’s another reasonable avenue of study. That’s unlikely to be the end of the story. Neuroscientist Keith Fargo of the Alzheimer’s Association, not involved in the research, tells Rosenbaum that a lot of genetic factors are also at play in the disease, and it will take more studies to untangle how immune reactions, genetics and other factors play into its progression.