Two common herpes viruses seem to play a role in Alzheimer's disease.

    Abdulaziz Sobh


    Researchers find herpes virus in brains marked by Alzheimer's disease

    Viruses, best known for causing a distinct skin rash in young children, are abundant in the brain tissue of people with Alzheimer's disease, a team of scientists reported Thursday in Neuron. The team also found evidence that viruses can interact with brain cells in ways that could accelerate the disease.

    "Our hypothesis is that they put the gas in the flame," says Joel Dudley, author of the study and associate professor of genetics and genomics at the Icahn School of Medicine in Mt. Sinai in New York City.

    The finding adds credibility to an idea decades ago that an infection can cause Alzheimer's disease. It also suggests that it is possible to prevent or delay Alzheimer's by using antiviral drugs or medications that modulate how immune cells in the brain respond to an infection.

    But the study does not prove that herpes viruses are involved in Alzheimer's, says Dr. Richard Hodes, director of the National Institute on Aging, which helped fund the research.

    "The data is very provocative, but it does not show a direct causal role," he says. "And if viral infections play a role, they are not the only actor."

    Still, the study offers strong evidence that viral infections can influence the course of Alzheimer's, says Hodes.

    Like many scientific discoveries, this was an accident. "Viruses were the last thing we were looking for," says Dudley.

    He and a team of researchers were using genetic data to look for differences between healthy brain tissue and brain tissue from people who died with Alzheimer's.

    The objective was to identify new targets for drugs. Instead, the team continued to find indications that brain tissue from Alzheimer's patients contained higher levels of the virus.

    "When we started to analyze the differences, he just yelled at us for the data," says Dudley.

    The team discovered that the levels of two human herpes viruses, HHV-6 and HHV-7, were up to twice as high in the brain tissue of people with Alzheimer's. They confirmed the finding by analyzing data from a consortium of brain banks.

    These herpes viruses are extremely common and can cause a rash called roseola in young children. But viruses can also enter the brain, where they can remain inactive for decades.

    Once researchers knew that viruses were associated with Alzheimer's disease, they began to try to discover how a virus could affect the course of a brain disease. That meant identifying the interactions between the genes of the virus and other genes in brain cells.

    "We have mapped the social network, if you will, from which genes the viruses are friends and who they are talking to inside the brain," says Dudley. In essence, he says, they wanted to know: "If the viruses are tweeting, who is tweeting?"

    And what they found was that the genes of the herpes virus were interacting with genes that increase the risk of Alzheimer's.

    They also discovered that these Alzheimer's risk genes seem to make a person's brain more vulnerable to infection with the two herpes viruses.

    But just having the herpes virus present in the brain is not enough to cause Alzheimer's disease, says Dudley. Something needs to activate the viruses, which makes them begin to replicate.

    It is not clear what causes the activation, says Dudley, although he suspects some kind of change in the internal functions of the brain cells.

    Once the viruses become active, they seem to influence things like the accumulation of plaques and tangles in the brain associated with Alzheimer's. "They're throwing a key at work," he says.

    Herpes viruses also seem to trigger an immune response in certain brain cells, says Hodes. These cells are part of an ancient immune system that has previously been implicated in Alzheimer's.

    Most previous efforts to prevent or treat Alzheimer's have been to try to reduce the plaques and tangles associated with the disease. Those efforts have failed to improve brain function even when they achieved their immediate goal.

    These "distressing and disappointing failures" suggest that it is time for new approaches, says Hodes. And the new study suggests at least two.

    One is to administer antiviral drugs to people with high levels of herpes virus in their brains. The Institute on Aging is already funding a study to test this approach in people in the early stages of Alzheimer's disease, says Hodes.

    Another approach is to prevent immune cells in the brain from reacting to the virus in a way that accelerates Alzheimer's, says Hodes. That's complicated, he says, because simply disabling the brain's immune cells could be harmful.

    Even so, Hodes is optimistic.

    "The more we learn about the disease process and the more goals we can address," he says, "the more likely we are to reduce or prevent the progression of Alzheimer's disease."


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