In a new study, researchers found evidence that refutes the link between increased levels of herpes virus and Alzheimer’s disease.
The research was conducted by a team at Baylor College of Medicine.
About 50 million people worldwide are affected by Alzheimer’s disease, a type of progressive dementia that results in the loss of memory, cognitive abilities and verbal skills, and the numbers are growing rapidly.
Currently available medications temporarily ease the symptoms or slow the rate of decline, which maximizes the time patients can live and function independently.
However, there are no treatments to halt the progression of Alzheimer’s disease.
Like all types of dementia, Alzheimer’s disease is characterized by the massive death of brain cells, the neurons.
Identifying the reason why neurons begin and continue to die in the brains of Alzheimer’s disease patients is an active area of research.
One theory that has gained traction in the past year is that certain microbial infections, such as those caused by viruses, can trigger Alzheimer’s disease.
A 2018 study reported increased levels of human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) in the postmortem brain tissues of more than 1,000 patients with Alzheimer’s disease when compared to the brain tissues of healthy-aging subjects or those suffering from a different neurodegenerative condition.
The presence of elevated levels of the genetic material of herpes viruses indicated active infections, which were linked to Alzheimer’s disease.
In less than a year, this study generated a flurry of excitement and led to the initiation of several studies to better understand the link between viral infections and Alzheimer’s disease.
Surprisingly, when the team reanalyzed the data sets from the 2018 study using the identical statistical methods with rigorous filtering, as well as four commonly used statistical tools, they were unable to produce the same results.
Moreover, the p-values did not fit with simple logistic regression—a statistical analysis that predicts the outcome of the data as one of two defined states.
In fact, after several types of rigorous statistical tests, they found no link between the abundance of herpes viral DNA or RNA and the likelihood of Alzheimer’s disease in this cohort.
This study highlights one of the potential pitfalls of over-reliance on p-values. While p-values are a very valuable statistical parameter, they cannot be used as a stand-alone measure of statistical correlation.
Data sets also have to be used in conjunction with accurately calculated p-values to make gene-disease associations that are statistically correct and biologically meaningful.
One author of the study is Dr. Zhandong Liu, an associate professor of pediatrics at Baylor.
The study is published in the journal Neuron.
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