Scientists have found up to two times higher level of human herpes virus among people with Alzheimer’s disease, suggesting the potential role of the viruses in the development of the progressive brain disorder.
Herpes virus causes contagious sores, most often around the mouth or on the genitals.
The study found unusually increased level of human herpesvirus named human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7 ) in the brains of the people with Alzheimer’s than those without the disorder.
“The hypothesis that viruses play a part in brain disease is not new, but this is the first study to provide strong evidence,” said Richard J. Hodes, Director from the US National Institutes of Health.
“Our work identified specific biological networks that offer new testable hypotheses regarding the role of microbial defense and innate immune function in the pathophysiology of Alzheimer’s,” said Joel Dudley from the Institute for Next Generation Healthcare at the Icahn School of Medicine at Mount Sinai.
The findings also showed multiple points of overlap between virus-host interactions and genes associated with Alzheimer’s risk. Multiple viruses impact the biology of Alzheimer’s disease across domains such as DNA, RNA and proteins.
“If it becomes evident that specific viral species directly contribute to an individual’s risk of developing Alzheimer’s or their rate of progression once diagnosed, then this would offer a new conceptual framework for understanding the emergence and evolution of Alzheimer’s at individual, as well as population, levels,” Dudley explained.
In the study, published in the journal Neuron, the team initially performed RNA sequencing on four brain regions in more than 600 samples of postmortem tissue from people with and without Alzheimer’s to quantify which genes were present in the brain, and whether any were associated with the onset and progression of Alzheimer’s.
Using different computational approaches, the team uncovered a complex network of unexpected associations, linking specific viruses with different aspects of Alzheimer’s biology.
They examined the influence of each virus on specific genes and proteins in brain cells, and identified associations between specific viruses and amyloid plaques, neurofibrillary tangles, and clinical dementia severity.
Further, they incorporated 800, RNA sequencing samples and observed a persistent increase of HHV-6A and HHV-7 in samples from individuals with Alzheimer’s. (IANS)