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VBCR - June 2015, Volume 4, No 3 - CCR Conference Highlights
Chase Doyle

Microglia may serve a protective purpose for the masses, but for those who suffer from fibromyalgia, these adaptive cells of the central nervous system are the enemy—the source of constant flu-like sickness and pain. Until recently, there has been little hope for defense.

According to research presented at the 2015 annual Congress of Clinical Rheumatology, however, scientists are beginning to understand the mechanisms behind this pain, offering the promise of an effective treatment for fibromyalgia, with implications that extend far beyond this crippling disease.

“I think the evidence is strongly supporting the role of microglia in fibromyalgia, chronic fatigue, major depression, and a lot of other neurological conditions and disorders,” said Jarred Younger, PhD, associate professor in the departments of Psychology, Anesthesiology, and Rheumatology, and director of the Neuroinflammation, Pain and Fatigue Lab, at the University of Alabama at Birmingham. “I think this is going to be the next huge advance in treatment when we figure out how to manipulate these microglia cells.”

According to the National Fibromyalgia Association, an estimated 10 million people are afflicted with fibromyalgia in the United States alone. The victims of this disease are mostly women, and prognosis is poor in terms of improvement.

“It’s still a mysterious disorder,” said Younger. “We don’t have any objective test that says, ‘yes, you have this disorder.’ So, it’s frustrating for the patients, and it’s frustrating for the physicians. We just don’t have the tools to treat this effectively.”

In Younger’s opinion, fibromyalgia is caused by neuroinflammation in the central nervous system, and the key to treating it is reducing the inflammatory process in the brain. None of the current US Food and Drug Administration–approved therapies, however, directly target these processes.

“We’re going to have to develop and discover and employ both pharmaceutical treatments and other interventions that can get to the central nervous system and target the cells that drive the inflammation,” he said.

And that means microglia, the brain’s cellular defense against invasion—fast-acting sentinels whose hypervigilance in people with fibromyalgia causes far more harm than good. In the so-called “primed state” of overexpressed receptors, these cells are acting on a hair trigger—fine for fleeting threats, but detrimental over time.

“They’re kind of like an angry drunk who’s looking for a fight,” said Younger.

And, if they are activated long enough, it pushes the central nervous system to a neurodegenerative state.

“There’s a lot of approaches to manipulating these microglial cells,” he said. “Probably the one with the most supporting data right now is naltrexone, but we need to work on more because it’s not going to help everybody.”

As Younger explained, scientists are not locked in to any particular modalities of research. Hypotheses are still evolving alongside the quest for new drugs, and even older therapies could play a role.

“We have all these anti-inflammatories, but they generally work in the peripheral nervous system,” he said. “If we could modify one of those peripheral anti-inflammatories, just to assist it to get into the central nervous system, that may be all we need.”

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Last modified: June 26, 2015
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