Recently, we have discussed potential alternatives to the amyloid hypothesis, including the complications of diabetes. According to this hypothesis, the accumulation of amyloid beta in the brain drives the progression of Alzheimer’s. Although amyloid beta does appear to contribute to this neurodegenerative disease, many experts are focusing their attention elsewhere.
After all, clinical trials over the past decade have specifically targeted this theory, leading to a failure rate of 99.6 percent. Now studying an old theory, research recently found that those who developed Alzheimer’s showcased twice the level of herpes virus than those living without this disease.
New Insight Into a Controversial Theory
In the past, there has not been any strong evidence that viruses, specifically herpes, causes Alzheimer’s. However, a recent paper, published in the journal Neuron, is bringing attention to this old theory. Opening a new potential avenue for finding the cause of Alzheimer’s, this research has raised some questions.
After studying 622 brains from people who had signs of Alzheimer’s, it was found that the level of herpes virus was double, in comparison to the 322 people who did not display signs of Alzheimer’s. Concentrations of herpes virus were found in regions associated with Alzheimer’s. In addition, the virus appeared to trigger genes that increase Alzheimer’s risk.
Although this is an exciting discovery, it was an accidental observation. The researchers did not set out to find this association. Instead, the researchers were studying drugs that could potentially treat Alzheimer’s patients. This concept was first discussed in the 1950s, as a number of researchers believed that Alzheimer’s was a “slow virus disease.”
Studying brains from three separate brain banks, the two strains of interest are HHV-6A and HHV-7. These strains are not as prevalent in the brains of patients living with other neurodegenerative conditions. These are not the strains that are sexually transmitted or the strains that cause cold sores.
However, they are highly common and for the most part, are symptomless. Infecting approximately 90 percent of children, this virus may degrade neurological processes after lying dormant for decades. To better understand the role of herpes, researchers will need to continue studying the impact that viruses have on human DNA and the growth of amyloid beta.
A Second Study Strengthens This Theory
In a second study, conducted by a team from Harvard University and Massachusetts General Hospital, it was found that herpes activated the growth of amyloid plaques. In this case, amyloid may act as the brain’s natural defense system against herpes and other viruses. This may lead to the misfiring of amyloid as Alzheimer’s progresses.
This has led researchers to believe that viruses and other microbes could be the “prequel” to the prevalent amyloid beta hypothesis. As amyloid continues to accumulate, the brain cannot successfully clear it out. To their surprise, the scientists also found that genes that are active in Alzheimer’s pathology may be active in order to fight viruses.
Since Alzheimer’s is such a complex disease, the researchers agree that the cause will not likely be one thing. It does appear that infectious agents may play a role in Alzheimer’s, including viruses. Based on these recent findings, we will continue to follow this theory as new developments unfold.
Could Antiviral Drugs Improve Symptoms of Alzheimer’s?
If viruses do contribute to the progression of Alzheimer’s, antiviral drugs could potentially impact the progression of this disease.
In a 2011 study, researchers from the University of Manchester further investigating previous findings. After finding that the herpes simplex virus type 1 (HSV1) is a risk factor for Alzheimer’s, the researchers began to focus on a potential intervention.
Since HSV1 may cause toxic amyloid plaques, the researchers studied antiviral agents based on their ability to target the replication of HSV1 DNA. The researchers treated HSV1-infected cells with acyclovir (the most commonly used antiviral drug). What they found, was that the accumulation of amyloid beta and phosphorylated tau decreased.
As the connection between Alzheimer’s disease and viral damage strengthen, new research avenues will develop. This could lead to clinical trials in humans that are unique in comparison to past trials, most of which failed.
Worried About Your Level of Thinking Today?
If you or a loved one are displaying potential early warning signs of Alzheimer’s or another form of dementia, we recommended the BrainTest® app. This assessment tool will help you detect possible cognitive impairments. Based on your results, you can then discuss your concerns with a physician.
After receiving an initial “report card,” these baseline results will also allow you to track your memory and level of thinking across time. You may read about the science behind this self-administered app here.