Around 44 million people around the world have Alzheimer’s disease, a progressive form of dementia that leads to memory loss and a decline in cognitive ability. In 2018, a study supported a link between having various forms of the herpes virus and Alzheimer’s disease. But is this really the case?
For the study, researchers analyzed the brain tissue of over 1,000 patients with Alzheimer’s disease postmortem, and then compared them to those of healthily-aging subjects and those with different neurodegenerative conditions. In the end, they found that those with Alzheimer’s had significantly higher levels of human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) in their brain tissue than those without the condition. Indicative of an active infection, the researchers concluded an association between HHV and Alzheimer’s.
However, a year on, when the researchers re-analyzed their data, they could not generate the same results. Co-author of the study, Dr. Hyun-Hwan Jeong said, “Our study highlights one of the potential pitfalls of over-reliance on p-values (the probability of getting the observed results of a test, given a correct null hypothesis). While p-values are a very valuable statistical parameter, they cannot be used as a stand-alone measure of statistical correlation - data sets from high-throughput procedures still need to be carefully plotted to visualize the spread of the data.”
Despite this review, other evidence still suggests a link between HHV and Alzheimer’s, although rather than directly causing it, these studies suggest that it may catalyze its development. For example, a study looking at data from Taiwan’s National Health Insurance Research Database found that those diagnosed with herpes simplex virus (HSV) were 2.56 times more likely to develop dementia in the future when compared to those undiagnosed. The data also showed that those diagnosed with an HSV infection who took antiviral medication to combat it were 90% less likely to develop dementia later on than those left unmedicated.
When looking at why this may be the case, researchers suggested that reactivation of HSV in elderly people under a lot of stress and with compromised immune systems may increase rates of inflammation in the brain. Another possibility is that HSV may accelerate beta-amyloid deposition, something that would leave the brain more vulnerable to infection, and perhaps contribute to the incidence of dementia.