Authors: Alice Weatherston
Increased levels of inflammation have previously been identified in approximately one third of individuals diagnosed with depression. A recent study published in Molecular Psychiatry has explored this association more fully and suggests that persistent inflammation has a direct impact on areas of the brain associated with long-term and often difficult to treat symptoms of depression, such as anhedonia.
The study, which was carried out by a team of researchers based at Emory University School of Medicine (GA, USA) and Winship Cancer Institute (GA, USA), collected MRI data from 48 patients with a depression diagnosis, in order to analyze functional connectivity. During the brain imaging section of the study, participants did not consume antidepressants, anti-inflammatory drugs or other medications for at least four weeks and levels of the inflammatory marker, C-reactive protein (CRP) were collected and recorded on each visit to ensure they were stable.
Results linked high levels of the CRP with a ‘failure to communicate’ between brain regions important for both motivation and reward. Specifically, patients exhibiting high CRP had reduced connectivity between the ventromedial prefrontal cortex and the ventral striatum. Those with low CRP had robust connectivity.
“We were interested in these regions of the brain because of their known importance for response to reward,” explained Jennifer Felger (Emory University School of Medicine and Winship Cancer Institute), lead author of the study. “In addition, we had seen reduced activation of these areas in people receiving immunostimulatory treatments for hepatitis C virus or cancer, which suggested that they may be sensitive to inflammation.”
In addition to these findings, high levels of CRP were correlated with reports of anhedonia, a symptom of depression some patients continue to experience even after beginning treatment with antidepressants.
Importantly, the results of the study reinforce the opinion that the high-inflammation form of depression is distinct. The team therefore now plan to investigate treatments targeted to the inflammation.
In particular, previous research in non-human primates has highlighted the Parkinson’s drug L-DOPA as a potential treatment, working through increasing levels of dopamine within the brain, a neurotransmitter often reduced as a result of inflammation. Felger and her team now hope to test whether L-DOPA can effectively increase connectivity in reward-related brain regions in individuals with high-inflammation depression.
“Some patients taking antidepressants continue to suffer from anhedonia,” Felger commented. “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.”
Source: Emory University press release