New research suggests, that viruses may play a role in the development of Alzheimer’s. Scientists say that while these findings don’t necessarily prove that viruses actually cause Alzheimer’s or that they are contagious, they do think that they will re-ignite some of the long-debated theories as to what actually triggers this disease.
The team led by researchers from New York's Mount Sinai Health System discovered that certain viruses can affect the way Alzheimer’s genes behave — two of these viruses included two very common herpes viruses.
The thought that infections earlier in someone’s life may in fact predispose them to Alzheimer’s years later has been a consideration by some mainstream medical researchers for years.
However, the prevailing theory that Alzheimer’s is caused by sticky plaques that clog the brain has overshadowed the virus theory.
But these new findings are beginning to sway some specialists to at least consider infections as a potential cause, especially since the previous attempts to block the beta-amyloid plaques has failed.
According to Dr. John Morris, "With an illness this terrible, we cannot afford to dismiss all scientific possibilities," Dr. Morris directs the Alzheimer's research center at Washington University School of Medicine in St. Louis.
And Dr. Rudolph Tanzi of Massachusetts General Hospital says that this new study fits with the mounting evidence that the aggressive nature used by the brains immune system to defend itself may in fact be riskier than the actual infection.
Along with his colleague Dr. Robert Moir from Harvard, Dr. Tanzi has performed experiments that show how sticky beta-amyloid captures and engulfs invading germs— which appears to be the reason why plaques form in the first place.
Dr. Tanzi went on to explain, "the question remained, OK, in the Alzheimer brain what are the microbes that matter, what are the microbes that trigger the plaque?"
The study funded by the National Institutes of Health started off looking for new drug targets for Alzheimer’s. The researchers from Mount Sinai and Arizona State came up with the viral suspects by accident.
By using complex genetic data from hundreds of brains at a variety of brain banks researchers compared differences between people who had died with Alzheimer’s and those that were considered to have normal cognitive function.
Mount Sinai geneticist Joel Dudley, one of the studies senior authors says that the first clues that viruses were around "came screaming out at us”.
Viral genetic material was found at far higher levels of the brain in those with Alzheimer’s when compared with the normal brains.
Two types of human herpes viruses, known as HHV6a and HHV7 were the most abundant. These viruses typically affect children and most often have no symptoms associated with them. Once they run their course they typically remain dormant in the body.
These findings were nothing new, as early as 1980 other researchers have linked a variety of bacteria and viruses to an increased risk of Alzheimer’s. Included in these viruses was another type of herpes that causes cold sores.
One thing researchers have never been able to conclude is whether these viruses are simply innocent bystanders or play an active role in triggering Alzheimer’s.
This new study however takes it a step further.
Using computer models to determine how the virus genes interacted with human genes, proteins and amyloid buildup researchers were able to see further into the process.
"We're able to see if viral genes are friending some of the host genes and if they tweet, who tweets back," Dudley said using a social media reference.
They were able to see a lot of interactions that suggested that the viruses even had the capability to switch on and off the Alzheimer’s – related gene.
In efforts to determine if these interactions made any difference, the researchers specifically bred mice lacking one molecule that herpes depletes.
As expected, those animals developed more plaques.
Keith Fargo, Alzheimer's Association scientific programs director, said, "I look at this paper and it makes me sit up and say, 'Wow”.
This research makes a viral connection much more likely, but he cautioned that the study won't affect how today's patients are treated.
However, Dr. Miroslaw Mackiewicz of NIH's National Institute on Aging says, If the findings pan out, they could change how scientists look for new ways to treat or prevent Alzheimer's. The NIH is already funding a new study to see if an antiviral drug benefits people who have both mild Alzheimer's and different herpes viruses.
Just having a herpes virus "does not mean you're going to get Alzheimer's," Mass General's Tanzi warned. It may not even have penetrated the brain.
But, in a new study that is set to be published in the near future, Dr. Tanzi was able to show how HHV6 and a cold sore – causing herpes virus can in fact trigger or "seed" amyloid plaque formation, supporting the Mount Sinai findings.
Regardless, he has his doubts that viruses are entirely to blame.
He says, "the Mount Sinai paper tells us the viral side of the story. We still have to work out the microbe side of the story”.
In separate research Tanzi, is looking for bacteria and other bugs in what's called the Brain Microbiome Project.
Dr. Tanzi says, "the brain was always thought to be a sterile place. It's absolutely not true."