New Evidence for a Controversial Alzheimer's Theory
For decades, research into treatments for Alzheimer's Disease has run into dead end after dead end. We don't know how to definitively prevent the chronic neurodegenerative disease, nor how to treat it with consistent efficacy, despite billions spent on research each year. A sense of futility has started to spread, prompting some to rethink common theories and others to throw up their hands in resignation. This year, the pharmaceutical company Pfizer ended research into Alzheimer's treatments altogether.
Conventional theories of Alzheimer's blame buildups of the starchlike protein amyloid for gumming up and ransacking the brain, but clinical trials testing methods that reduce amyloid plaques have been repeatedly unsuccessful at halting the disease. It's starting to seem more likely that amyloid buildups are a response to the disease, not the cause.
An outside-the-box theory received new attention in an extensive study published today to the journal Neuron. Researchers based out of the Icahn School of Medicine at Mount Sinai, the National Institutes of Health, and Arizona State University cooperated on numerous analyses to implicate herpesviruses, and particularly one called HHV-6, as having a possible role in Alzheimer's Disease.
HHV-6 and its close sibling HHV-7 infect more than 90% of people in North America by the time they are a few years old. Infections are almost entirely asymptomatic, although they can cause the mild childhood disease Roseola, characterized by a fever and rash usually lasting no more than a few days.
Considering HHV-6's relatively innocuous reputation, the researchers behind the current study were surprised that it could be involved in Alzheimer's, perhaps the most insidious disease in the Western world.
"We didn't set out to find what we found. Not even close. We were trying to find drugs that could be repurposed to treat Alzheimer's patients, but the patterns that emerged from our data-driven analysis all pointed towards these viral biology themes," co-senior author and Arizona State geneticist Joel Dudley said in a statement.
Dudley and his co-authors were examining a bounty of brains from deceased patients with brain disorders and stumbled upon a number of curious correlations. For starters, HHV-6 DNA and RNA were highly concentrated in the brains of those diagnosed postmortem with Alzheimer's disease. At the same time, HHV-6 was not as abundant in the brains of those with other neurodegenerative disorders. Subsequent analyses revealed that the herpesvirus genes were interacting with genes associated with risk for Alzheimer's Disease.
The present findings are thorough, but do not definitively implicate herpesviruses as the cause of Alzheimer's disease. It's still possible that HHV-6 viruses are merely opportunistic agents, infecting brains already weakened by disease. Still, given the current bleak landscape of Alzheimer's treatment research, herpesviruses are definitely worth investigating further. Treatments that somehow reduce these pathogens in a diseased brain might just yield the positive results that tens of millions of people have been hoping for.
Source: Neuron, Readhead et al.: "Multiscale Analysis of Independent Alzheimer's Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus"