Researchers say that persistent and high inflammation in the brain affects connections relating to important symptoms that are currently difficult to treat, triggering up to a third of all cases of depression. And they believe their discovery can point to other therapeutic remedies for depression (CLICK HERE TO READ FULL STUDY)
Researchers from Emory University School of Medicine say that persistent and high inflammation in the brain affects connections relating to important symptoms that are currently difficult to treat, triggering up to a third of all cases of depression. And they believe their discovery can point to other therapeutic remedies for depression, which afflicts hundreds of millions of people who frequently are resistant to the current drugs available for the disease.
In a study published in Molecular Psychiatry this month, researcher Jennifer Felger and colleagues linked anhedonia–the inability to achieve pleasure–to inflammation that causes the “failure to communicate” between two areas of the brain known as the ventral striatum (VS) and ventromedial prefrontal cortex (vmPFC).
“Some patients taking antidepressants continue to suffer from anhedonia,” says Felger. “Our data suggest that by blocking inflammation or its effects on the brain, we may be able to reverse anhedonia and help depressed individuals who fail to respond to antidepressants.”
The “failure to communicate” between the VS and vmPFC brain regions that control motivation and reward was picked up by MRI imaging in 48 patients with depression. Interestingly, these brain images were correlated with the inflammatory marker CRP (C-reactive protein) in these patients compared to non-depressed individuals.
CRP is a valuable marker since it is found in the blood, making it relatively easy and convenient to test its levels in the clinic.
The finding followed from an initial observation that patients receiving an immuno-stimulatory treatment for hepatitis C virus or cancer showed the same reduced activation of these brain areas. Since this class of drugs increases inflammation, they correlated the two together after controlling for other variables.
Felger and her team have previously shown that inflammation reduces levels of dopamine release in the brains of nonhuman primates. Their next step is to test whether L-DOPA, a precursor drug of the brain chemical dopamine, can increase the connection between the VS and vmPFC brain regions in patients with high-inflammation depression. That study will be supported by the Dana Foundation.