Alzheimer’s may be triggered by a virus, according to a new study that discovered people with the disease had twice the level of the common herpes bug.
Researchers say their findings suggest that a controversial hypothesis that viruses are involved in dementia may be correct.
The American team found ‘unusually high’ levels of two strains of human herpes virus 6A (HHV-6A) and human herpes virus 7 (HHV-7) in brains of Alzheimer’s sufferers compared to those free of the disease.
And the findings offers potential new paths for the early treatment to prevent the disease.
The findings were based on a large-scale analysis at three different brain banks by researchers from the Icahn School of Medicine at Mount Sinai and Arizona State University-Banner Neurodegenerative Disease Research Center (NDRC).
The nature and significance of viruses and other pathogens in the brain are currently hot topics in neuroscience, though the exploration is still in its early stages.
One of the primary questions is whether such pathogens play an active, causative role in the disease or enter the brain simply as opportunistic passengers, taking advantage of the neural deterioration characteristic of Alzheimer’s disease.
Senior author Associate Professor Joel Dudley, at Icahn, said: “Previous studies of viruses and Alzheimer’s have always been very indirect and correlative.
“But we were able to perform a more sophisticated computational analysis using multiple levels of genomic information measured directly from affected brain tissue.
“This analysis allowed us to identify how the viruses are directly interacting with or coregulating known Alzheimer’s genes.
“I don’t think we can answer whether herpesviruses are a primary cause of Alzheimer’s disease.
“But what’s clear is that they’re perturbing and participating in networks that directly underlie Alzheimer’s pathophysiology.
“This study represents a significant advancement in our understanding of the plausibility of the pathogen hypothesis of Alzheimer’s.
“Our work identified specific biological networks that offer new testable hypotheses regarding the role of microbial defence and innate immune function in the pathophysiology of Alzheimer’s.
“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.”
The study was the first to use a data-driven approach to study the impact of viruses on Alzheimer’s and to identify the role of HHV-6A and HHV-7 in the disease. T
It was also the first evidence that integration of HHV genomes into human brain genomes may play a role in the etiology of Alzheimer’s.
The viruses can cause encephalitis and other chronic conditions.
The findings were based on RNA sequencing on four brain regions in more than 600 samples of postmortem tissue from people with and without Alzheimer’s.
This quantified which genes were present in the brain, and whether any were associated with the onset and progression of Alzheimer’s.
The researchers believed the findings back up previous research on the role of innate immunity in the disease, particularly recent findings that beta-amyloid protein – the culprit behind the plaques that build up in the Alzheimer’s-affected brain – may accumulate as part of a defence against infections.
The study found that herpes viruses were involved in networks that regulate amyloid precursor proteins.
But people should not be worried by the findings.
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.”
This is especially true because HHV-6A and HHV-7 are extremely common and often latent or asymptomatic.
In the US nine in ten children have one of these viruses circulating in their blood by the time they’re a few years old.
But even if questions remain, the research offered strong support for a long-controversial hypothesis that viruses might be involved in the development of Alzheimer’s disease.
Prof Dudley said: “We didn’t have a horse in this virus race whatsoever. It’s the data that took us there.
“And 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.”
Prof Dudley noted the study could potentially translate to the identification of virus, or virus-related, biomarkers that could improve patient risk stratification and diagnosis, as well as implying novel viral targets and biological pathways that could be addressed with new preventative and therapeutic drugs.
Study author Professor Dr Sam Gandy added: “This is the most compelling evidence ever presented that points to a viral contribution to the cause or progression of Alzheimer’s.”
The study was published in the journal Neuron.
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