A drug that enhances the effects of dopamine inflammation on the brain in depression

Study shows that levodopa, a drug that increases dopamine in the brain, has the potential to reverse the effects of inflammation on the brain’s reward circuits, improving symptoms of depression

Numerous labs around the world have shown that inflammation reduces motivation and anhedonia, one of the main symptoms of depression, by affecting reward pathways in the brain. Previous research from the Department of Psychiatry and Behavioral Sciences at Emory University School of Medicine has linked the effects of inflammation in the brain with decreased release of dopamine, a chemical neurotransmitter that regulates motivation and motor activity in the ventral striatum.

At the nature studyresearchers showed that levodopa reversed the effects of inflammation on functional brain connectivity in reward circuits and anhedonia (inability to experience pleasure) in depressed individuals with higher levels of C-reactive protein (CRP), a biomarker produced and released by the liver in response to inflammation.

Inflammation levels can be easily measured using simple blood tests such as PCR, which are readily available in clinics and hospitals. The study included 40 depressed patients with CRP levels ranging from high to low, who underwent functional brain scans at two visits after receiving randomly prescribed placebo or levodopa, a drug often prescribed for disorders such as Parkinson’s disease.

depression and inflammation

Levodopa improved functional connectivity in a classical reward circuit between the ventral striatum and the ventromedial prefrontal cortex, but only in patients with higher levels of CRP. This improvement in the reward circuit in depressed individuals with higher CRP was also correlated with a reduction in anhedonia symptoms after levodopa.

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According to principal investigator and lead author, Jennifer C. Felger, “This research demonstrates the translational potential for using inflammation-related deficits in functional connectivity and may have important implications for future investigations of precision therapies for psychiatric patients with high inflammation.

Felger says the study results are crucial for two reasons. First, they suggest that depressed patients with heightened inflammation may specifically respond to drugs that increase dopamine. Second, Felger adds that these findings also provide additional evidence that functional connectivity in reward circuits can serve as a reliable brain biomarker for the effects of inflammation in the brain.

“Moreover, as the effect of levodopa was specific for depressed patients with increased inflammation, this functional connectivity can be used to assess the brain’s responsiveness to new treatments that may target this subtype of depressed patients in future studies and clinical trials,” says Felger. .

Emory Brain Health research is contributing to a growing international literature reporting reproducible relationships between inflammation and poor functional connectivity in reward circuits, as well as other important regions and networks relevant to symptomatic domains such as anhedonia that are common to depression and other illnesses. psychiatric.

REFERENCE

Functional connectivity in the reward circuit and anhedonia symptoms as therapeutic targets in depression with high inflammation: evidence from a dopamine provocation study

Source: Emory University

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