Research 'most compelling evidence ever' of viral trigger for Alzheimer's

23 June, 2018, 02:47 | Author: Lillian Steele
  • GETTY ImagesDementia Alzheimer's supplement to prevent symptoms is'important medical advancement

Human herpesvirus 6A (HHV-6A) and human herpesvirus 7 (HHV-7) were found in postmortem Alzheimer's disease samples at levels up to twice as high as non-Alzheimer's disease samples, Ben Readhead, MBBS, of Icahn School of Medicine at Mount Sinai in New York City, and colleagues reported in Neuron.

The researchers analysed data from three major brain banks courtesy of the National Institutes of Health's Accelerating Medicines Partnership - Alzheimer's Disease (AMP-AD) consortium, which allowed them to look at raw genomic data for large numbers of Alzheimer's patients in different cohorts.

"To date, research across the world has largely focused on studying the role of amyloid that appears in the brain of people with Alzheimer's disease".

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. Most abundant were two human herpes viruses, known as HHV6a and HHV7, that infect most people during childhood, often with no symptoms, and then lie dormant in the body. The study points to the viruses as possible accomplices that drive disease progression but does not suggest that Alzheimer's may begin after they are transmitted through casual contact.

The new study went farther: Researchers used computer models to check how the viral genes interacted with human genes, proteins and amyloid buildup, nearly like the viruses' social media connections, Dudley explained. "Collectively, these findings support the role of miR-155 as a key node in host response to AD-relevant viral perturbation, and as a potential mediator of neuronal loss", they state.

It is estimated that by 2050, almost 14 million Americans will be living with Alzheimer's disease. "What I believe is that in genetically or physiological susceptible individuals, the virus is acting as an agonist of the disease", Dudley says-a number of processes likely participate, with viruses being just one piece of the puzzle.

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Alzheimer's disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out simple tasks.

Using computational tools to analyze these large datasets, the researchers were able to generate a picture of the genetic, transcriptional, and molecular networks that underpin AD development and progression and how viruses are potentially involved. The team also found evidence that the viruses can interact with brain cells in ways that could accelerate the disease. About 90% of adults have been exposed to the herpes virus by age 50, research shows, and not all of them will go on to develop dementia. Their data analyses and subsequent studies in experimental mice found that the HHV-6A virus effectively suppressed miR-155, leading to altered levels of Aβ and amyloid plaque density in vivo. The strains have been linked to encephalitis and other chronic conditions.

If the findings eventually pan out, they could lead to new targets for Alzheimer's treatment.

The nature and significance of viruses and other pathogens in the brain are now hot topics in neuroscience, though the exploration is still in its early stages. Some studies have even tried to build a bridge between the two hypotheses, suggesting amyloid aggregation in the brain is stimulated by microbial infection. The plaques also alert brain immune cells called microglia to the fact that something is wrong; these cells launch an immune cascade that kills even more neurons.

Strengthening the evidence for this controversial idea will be hard. "This research reinforces the complexity of Alzheimer's disease, creates opportunities to explore Alzheimer's more thoroughly, and highlights the importance of sharing data freely and widely with the research community".

But Dudley is willing to accept the risks and push forward.

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