Researchers Find Herpes Viruses In Brains Marked By Alzheimer's Disease 
 
 Two common herpes viruses appear to play a role in Alzheimer's disease. 
 
 The viruses, best known for causing a distinctive skin rash in young children, are abundant in brain tissue from people with Alzheimer's, a team of scientists reports Thursday in Neuron. The team also found evidence that the viruses can interact with brain cells in ways that could accelerate the disease. 
 
 "Our hypothesis is that they put gas on the flame," says Joel Dudley, an author of the study and an associate professor of genetics and genomic sciences at the Icahn School of Medicine at Mt. Sinai in New York City. 
 
 The finding adds credence to a decades-old idea that an infection can cause Alzheimer's disease. It also suggests that it may be possible to prevent or slow Alzheimer's using antiviral drugs, or drugs that modulate how immune cells in the brain respond to an infection. 
 
 But the study doesn't 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 are very provocative, but fall short of showing a direct causal role," he says. "And if viral infections are playing a part, they are not the sole actor." 
 
 Even so, the study offers strong evidence that viral infections can influence the course of Alzheimer's, Hodes says. 
 
 Like a lot of scientific discoveries, this one was an accident. "Viruses were the last thing we were looking for," Dudley says. 
 
 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 goal was to identify new targets for drugs. Instead, the team kept finding hints that brain tissue from Alzheimer's patients contained higher levels of viruses. 
 
 "When we started analyzing the differences, it just sort of came screaming out at us from the data," Dudley says. 
 
 The team found that levels of two human herpes viruses, HHV-6 and HHV-7, were up to twice as high in brain tissue from 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 skin rash called roseola in young children. But the viruses also can get into the brain, where they may remain inactive for decades. 
 
 Once the researchers knew the viruses were associated with Alzheimer's they started trying to figure out how a virus could affect the course of a brain disease. That meant identifying interactions between the virus genes and other genes in brain cells. 
 
 "We mapped out the social network, if you will, of which genes the viruses are friends with and who they're talking to inside the brain," Dudley says. In essence, he says, they wanted to know: "If the viruses are tweeting, who's tweeting back?" 
 
 And what they found was that the herpes virus genes were interacting with genes known to increase a person's risk for Alzheimer's. 
 
 They also found 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 herpes virus present in the brain isn't enough to cause Alzheimer's, Dudley says. Something needs to activate the viruses, which causes them to begin replicating. 
 
 It's not clear what causes the activation, Dudley says, though he suspects some sort of change in the internal functions of brain cells. 
 
 Once the viruses do become active, they appear to influence things like the accumulation of the plaques and tangles in the brain associated with Alzheimer's. "They are sort of throwing a wrench in the works," he says. 
 
 The herpes viruses also seem to trigger an immune response in certain brain cells, Hodes says. 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 involved trying to reduce the plaques and tangles associated with the disease. Those efforts have failed to improve brain function even when they accomplished their immediate goal. 
 
 Those "distressing and disappointing failures" suggest it's time for some new approaches, Hodes says. And the new study suggests at least two. 
 
 One is to give 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, Hodes says. 
 
 Another approach is to prevent the brain's immune cells from reacting to the virus in ways that accelerate Alzheimer's, Hodes says. That's tricky, 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 targets we can address," he says, "the greater the probability we are going to slow or prevent the progression of Alzheimer's disease." 

 Alzheimer's disease affects millions of people around the world, but what ultimately causes the debilitating dementia remains unknown. One controversial theory, however, holds that the disease might be the result of a virus, or multiple viruses, infecting the brain. 
 
 Now, a new study offers more evidence to bolster this theory. In the study, published today (June 21) in the journal Neuron, researchers found that the brains of deceased people with Alzheimer's disease had higher levels of viruses than the brains of deceased people without Alzheimer's. Specifically, the Alzheimer's brains had up to twice as much of two common strains of herpes viruses than the non-Alzheimer's brains. [6 Big Mysteries of Alzheimer's Disease] 
 
 The theory that viruses or other pathogens could play a role in the development of Alzheimer's "is actually a pretty old idea," said lead study author Dr. Benjamin Readhead, an assistant research professor at Arizona State University and adjunct faculty member at the Icahn School of Medicine at Mount Sinai. "Even as early as the 1950s, people have been … positing the potential for some kind of pathogen to be contributing to Alzheimer's disease." Still, these ideas have received much backlash from scientists and medical experts throughout the years. 
 
 Readhead and his team didn't set out to look for possible viruses; rather, at first they were trying to find brain networks that existing drugs could be repurposed to target as potential treatments for the disease. "That actually kind of led us down this rabbit hole where we started suspecting that viruses could [explain] some of what we were seeing in these Alzheimer's disease networks," Readhead told Live Science. 
 
 In the study — one of the most detailed analyses of Alzheimer's brain tissue done to date — the team analyzed nearly 1,000 postmortem brains of people with and without Alzheimer's disease from multiple brain banks. They sifted through raw RNA and DNA sequences taken from these brain tissues and identified which of these genetic sequences were human and which were not. The non-human genetic sequences were compared to a database that contained genetic data for more 500 different viruses that researchers know can, or are thought to, affect humans. 
 
 Though the idea of a virus or bacterium playing a role in Alzheimer's development has not been historically well-regarded, previous research has looked at the idea. In particular, past research has pointed to connections between Alzheimer's disease and the herpes simplex virus one, or HSV1 (the form of herpes virus that typically causes cold sores). 
 
 But in the new study, two different strains of the herpes virus stood out: herpes 6A and herpes 7. 
 
 And while it may sound startling to learn that there are strains of herpes in the brain, "the thing to say about these viruses is that they're very, very common," Readhead said. (Nearly everyone carries these herpes strains in their bodies because they are infected with them in infancy. However, the strains don't typically cause problems other than rashes in young children.) In fact, the researchers detected the presence of these viruses in about 40 to 50 percent of the brain tissues examined in the study. But the Alzheimer's brain samples had many more copies of these viruses than those without, he said. 
 
 Because viruses were found in both Alzheimer's brain tissue and non-Alzheimer's brain tissue, the researchers can't "simply say that infection with these viruses causes Alzheimer's disease," Readhead said. "There's obviously some other important mechanisms that change why some people would have a different response to the presence of a virus." 
 
 Still, the viruses may play a role: They could be part of the cause, or they could also just serve to accelerate the disease, Readhead said. Or maybe they don't play a role at all, and just happen to be along for the ride, he added. 
 
 To better elucidate the role, if any, of the viruses, the researchers looked to see if any of the viruses were affecting proteins and genes known to be implicated in Alzheimer's. 
 
 "There were actually quite a few different viruses that we saw [connected] in some interesting ways to different aspects of Alzheimer's," Readhead said. For example, the herpes 6A virus was found to interact with a large number of genes linked to Alzheimer's disease risk, as well as genes related to amyloid plaques, which are protein clumps that form in the brains of people with the disease. 
 
 Still, more research is needed. "One of the real outstanding questions to this is trying to determine the extent [to which] what we're seeing could be a causal contributor to the disease," Readhead said. 
 
 Hugo Lövheim, a senior lecturer in the Department of Community Medicine and Rehabilitation at Umeå University in Sweden who was not part of the study, praised the new research. 
 
 "The authors have performed a really impressive in-depth analysis of postmortem Alzheimer’s disease brain tissue samples using modern bioinformatics techniques," Lövheim told Live Science. "This is in line with the now rapidly increasing evidence of viral infections as key drivers in the development of Alzheimer’s disease pathology." [9 Surprising Risk Factors for Dementia] 
 
 However, Lövheim noted that he still believes HSV1 "is a more likely cause of the disease" at its onset. The new study, along with some earlier research, he said, indicates that the herpes 6A virus may play a role at least in late Alzheimer’s disease. Therefore, future Alzheimer's drug research could aim to target both strains of the virus, he said. 
 
 Ruth Itzhaki, a professor emeritus of neuroscience and experimental psychology at the University of Manchester in England was also not a part of the new study, but was the first researcher to point to the possible role of HSV1 in Alzheimer's, back in 1991. 
 
 Itzhaki told Live Science in an email that she still thinks HSV1 has a stronger link to Alzheimer's, but that the viruses could be working together. 
 
 "It’s good that the viral concept is now being taken seriously, because during almost all of 28 years, I and subsequently others have suffered venomous hostility, derision or neglect from influential people in the field," she said. 
 
 Originally published on Live Science.
– It's not a we-figured-it-out moment, but it may be a clue. Scientists have discovered that two highly common herpes viruses tend to be present in an "increased" way in the brains of people who suffered from Alzheimer's, according to a study published Thursday in Neuron of nearly 1,000 postmortem brains. NPR reports the study also found HHV-6 and HHV-7 may "put gas on the flame," as study author Joel Dudley puts it, meaning the viruses' presence could be speeding up the progress of the disease. Now, the word of caution, from National Institute on Aging director Dr. Richard Hodes: "The data are very provocative, but fall short of showing a direct causal role. If viral infections are playing a part, they are not the sole actor." Dudley elaborates on that point, saying the presence of the viruses in the brain doesn't trigger Alzheimer's, but something—which isn't yet known—may be waking up the viruses and causing them to start replicating. The finding does suggest at least one course of action, which Hodes says the institute will be testing: dosing people who have high herpes levels in the brain with antiviral drugs. Live Science notes that "it may sound startling to learn that there are strains of herpes in the brain," but it really isn't. Lead study author Dr. Benjamin Readhead says nearly one of every two brain tissues analyzed had the viruses; it's just that the Alzheimer's brains had up to twice as much. The HHV-6 and HHV-7 strains don't typically cause issues beyond a skin rash called roseola that little kids can experience.