The cold sore virus, herpes simplex 1 (HSV-1), is often considered not much more than a nuisance for the estimated 67 percent of the world’s population believed to be infected.
However, the latest research shows HSV-1 might cause more health problems than we’re being led to believe, as science is linking the virus directly to Alzheimer’s disease in a lab model.
Now, this isn’t the first time that science has suggested a link between herpes and Alzheimer’s disease, but past research was often ignored in favor of the amyloid plaque theory of the disease. Scientists thought, we’ll just create a drug to clear away the sticky amyloid proteins and it’s “job done.”
Three decades and hundreds of failed drug trials later, the plaque-busting approach hasn’t moved us one inch closer to an effective treatment for Alzheimer’s disease.
Perhaps the latest research findings will finally convince them to steer another course.
In 1991, a molecular neurobiologist in England discovered HSV-1 in the brains of people who had died from Alzheimer’s disease and carried the most common gene for increased risk of the disease.
Nearly half a dozen journals refused to publish Dr. Ruth Itzhaki’s research before it was accepted by the Journal of Medical Virology. Dr. Itzhaki believed it was HSV-1 that killed brain cells, and amyloid plaques were the result. Peer reviewers didn’t agree, saying Dr. Itzhaki’s findings were too far outside the “Alzheimer’s mainstream.”
I didn’t know “being in the mainstream” was a step in the scientific method, but let us continue…
Now, a Tufts University study is backing up Dr. Itzhaki’s theory.
A Miniature Bioengineered Brain to Study Viral Assault
In groundbreaking work into Alzheimer’s disease, scientists and engineers led by Tufts University created a three-dimensional model of the human brain that’s only a fraction of an inch in size.
Starting with skin cells, genetic techniques were used to turn them into neural stem cells. These were grown on a donut-shaped, sponge-like scaffold. Four days later the entire menagerie of the brain had taken shape, transmitting and receiving electrical signals where neurons connect.
The model doesn’t replicate the brain’s structures; it’s what the scientists call a tissue-engineered system. Distinguished Professor in Engineering, David Kaplan, who led the research said it contained “amazing networks” and was “the whole deal.”
Once the model was up and running, it was infected with the herpes virus. What happened next was remarkable.
“After just three days of herpes infection,” reports Prof. Kaplan, “we saw large and dense plaque formations of beta amyloid protein, as well as increased expression of some of the enzymes responsible for generating the plaques.
“We observed neuron loss, neuro-inflammation and depressed signaling between neurons – everything we observe in patients. Never before have so many facets of the disease been replicated in vitro.”
The Virus Messes with DNA
Prof. Kaplan’s team also found that 40 genes known to raise the risk of Alzheimer’s were overexpressed compared to non-infected tissue, two of which are involved in producing the beta amyloid peptides found in plaques.
This is an example of epigenetics, in which outside factors – in this case a virus – turn various genes on or off.
As the professor explained, “These were profound changes, and all these responses — the physiological changes and the functional degradation — are important for the disease. And these were just normal cells. I don’t think anyone has shown these kinds of responses to HSV-1, not in a way that shows direct causality.”
The emphasis on normal cells is important because in studying Alzheimer’s scientists usually use genetic mutations to induce the human equivalent of the disease in culture or rodent models. The Tufts study demonstrates that herpes virus alone can induce the disease in normal cells.
The next test was to see what happened when they added valacyclovir, an anti-viral medication that’s prescribed for outbreaks of herpes.
Not only did the level of infection decrease, but the tissue became less inflamed, the amount of gunk jamming up the cells was reduced, and brain function improved.
Amyloid Plaques Defend the Brain
Four years ago, an international team of 31 senior scientists wrote a short article in the Journal of Alzheimer’s Disease describing solid evidence to suggest Alzheimer’s disease is caused by an infectious agent.
They were dismayed that this possibility was being ignored in favor of other approaches that grab all the research funds.
However, with the failure of yet another anti-amyloid drug one year ago, and critics of the amyloid approach becoming more vocal, more research is being directed at HSV-1 and other pathogens as the cause of Alzheimer’s disease. Funding has also started to flow from the National Institutes of Health (NIH) to studies like these.
For her part, Dr. Itzhaki, has continued researching the role of HSV-1 in Alzheimer’s ever since her groundbreaking study in 1991.
She said the Tufts model demonstrates directly what has previously only been inferred by observing a high incidence of herpes in dementia patients. The new study indicates that one actually causes the other: the virus can kick-start the disease process. The characteristic plaques and tangles are nothing more than a defensive response to the virus and not the cause.
A Potential Game-Changer
We have to see the Tufts finding confirmed in live subjects, but if it is (and I think it will be), the result could be a game-changer for dementia treatment.
According to the NIH, nine out of ten adults have been exposed to the herpes virus by age 50. Once infected, the virus lies dormant in a group of nerve cells for life.
Of course, nothing like that percentage will develop Alzheimer’s disease, so scientists can only speculate as to why the virus is triggered into action in the brain. They theorize that it could be factors relating to genetics, lifestyle, environmental conditions, and aging. Many people have the herpes virus without having any symptoms – or the symptoms they do have are mild or rare, occuring when they are generally run down and immune-compromised.
The research is just another reason to keep your immune system in tip-top shape. The stronger your immune system, the less likely you are to suffer the damaging effects of the herpes virus, or any other virus for that matter.