Herpes virus can lie dormant and then re-activate when someone's immune system is down, so it's not clear if the viruses cause Alzheimer's or if they re-activate as the disease progresses. I don't think we can answer whether herpesviruses are a primary cause of AD.
"The more we learn about the disease process and the more targets we can address", he says, "the greater the probability we are going to slow or prevent the progression of Alzheimer's disease".
Some scientists have long suspected viruses or bacteria somehow set the stage for Alzheimer's. "Now, not only is the viral hypothesis resurrected: it has specific testable pathways and networks and interactions that can be explored and reconciled with the rest of the work emerging in Alzheimer's", said study coauthor Joel Dudley, PhD, in a statement. Each patient had undergone clinical evaluation to follow the course of their disease before death and neuropathological evaluation to evaluate factors, including the degree of amyloid plaque formation.
The researchers confirmed their findings with sequencing samples collected by other brain banks, including the Mayo Clinic in Florida and the Religious Orders Study at Rush University in Chicago, observing a persistent abundance of HHV-6A and HHV-7 among Alzheimer's disease patients in those cohorts, too. Rather, the findings show viral DNA sequences and activation of biological networks-the interrelated systems of DNA, RNA, proteins and metabolites-may interact with molecular, genetic and clinical aspects of Alzheimer's.
Dr Riona Murray said: "Given our growing and ageing population and, importantly, that we live in a time when the nutritional value of foods continues to decline, I believe this is a valuable discovery that will challenge perceptions worldwide about the role of nutrition on brain function". "HHV-6A stood out as a notable", they state, and exhibited a significant overlap between the set of host genes it collectively induced across all tissues and AD-associated genes. When they later bred mice deficient in this microRNA, they found that the rodents developed larger and more abundant amyloid plaques in their brains than did mice with normal microRNA levels.
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The networks described suggest that the characteristic features of AD may arise as collateral damage that is caused in response to a viral assault.
Once the viruses do become active, they appear to influence things like the accumulation of the plaques and tangles in the brain associated with Alzheimer's.
The researchers were particularly interested in the microRNA (miRNA) miR-155, which has previously been linked with neuropathologic features of AD. In March 2016 in the Journal of Alzheimer's Disease, 33 global scientists penned an editorial urging the research community to seriously consider the idea that pathogens could be involved. But "more research is needed to discover exactly what roles, if any, they play".
Before that can happen, though, "we need to come up with better tools to identify those with Alzheimer's who have high-risk genetics who also have virus exposure in brain", Dudley added.
Co-senior author Professor Dr Sam Gandy said: "While these findings do potentially open the door for new treatment options to explore in a disease where we've had hundreds of failed trials, they don't change anything that we know about the risk and susceptibility of Alzheimer's disease or our ability to treat it today". Ruth Itzhaki, a neurobiologist at the University of Manchester in the United Kingdom, who has led numerous studies linking HSV-1 with Alzheimer's, says she has suffered "derision and vituperative hostility" for pursuing this line of inquiry.
A new study found those with the neurological disorder had twice the levels of two strains of herpes, HHV-6A and HHV-7, than those without the condition.