Summary: Levodopa, a drug commonly prescribed as a treatment for Parkinson’s disease, which increases dopamine in the brain, has been shown to improve symptoms associated with depression by altering the effects of the neurological disorder on the reward system.

Source: Emory University

Emory University published a study Molecular psychiatry Levodopa, a drug that increases dopamine in the brain, has been shown to have the potential to reverse the effects of inflammation on brain rewards, ultimately improving symptoms of depression.

Many laboratories around the world have shown that tumors can reduce motivation and anhedonia, a major symptom of depression, by affecting the brain’s reward pathways.

Previous research from Emory University School of Medicine’s Department of Psychiatry and Behavioral Sciences has linked the effects of inflammation on the brain to a reduction in the release of dopamine, a chemical neurotransmitter that controls motivation and motor activity in the ventral striatum.

In the study, researchers showed that levodopa alters the effects of levodopa on reward circuits and the functional connectivity of the brain, a blood biomarker developed and released in depressed people with anhedonia. Liver response to inflammation.

Levels of infection can be easily measured with simple blood tests such as CRP at clinics and hospitals across the US.

The study involved 40 depressed patients with high to low CRP levels who underwent functional brain scans at two visits after receiving either a placebo or levodopa, which is often prescribed for conditions such as Parkinson’s disease, in randomized order.

Levodopa improved functional connectivity in the classic ventral striatum to ventromedial prefrontal cortex reward circuit, but only in patients with high CRP levels. This improvement in reward perception in depressed subjects with higher CRP correlates with reduced symptoms of anhedonia after levodopa.

This shows a young man crying.
Levels of inflammation are easily measured with simple blood tests such as CRP, readily available in clinics and hospitals across the US. Image is in the public domain.

“This research demonstrates the translational potential of using inflammation-related deficits in functional correlates and may have important implications for future investigations into appropriate treatments for dementia patients with high inflammation,” said principal investigator and senior author Jennifer C. Felger, Ph. D., Associate Professor of Psychiatry and Behavioral Sciences, Emory School of Medicine.

Felger said the study’s findings are significant for two reasons. First, they suggest that depressed patients with high inflammation may respond to drugs that increase dopamine.

Second, Felger says these findings provide further evidence that functional connectivity in reward circuits can serve as a reliable brain biomarker of brain damage.

In addition, since the effect of levodopa is different for depressed patients with high inflammation, this functional relationship can be used in future studies and clinical trials to evaluate the brain response to new treatments aimed at this type of depressed patients. ” says Felger.

So psychopharmacology and depression research news

Author: Jennifer Johnson McEwen
Source: Emory University
Contact: Jennifer Johnson McEwen – Emory University
Image: The image is in the public domain.

Preliminary study: Open Access.
Functional connectivity in reward circuitry and symptoms of anhedonia as therapeutic targets in major depressive disorder: evidence from a dopamine challenge study.By Mandak Bkhbat et al. Molecular psychiatry


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Functional connectivity in reward circuitry and symptoms of anhedonia as therapeutic targets in major depressive disorder: evidence from a dopamine challenge study.

Increased inflammation in major depressive disorder (MDD) has been associated with lower functional connectivity (FC) in corticostriatal reward circuits and symptoms of anhedonia, a relationship that may involve inflammation synthesis and dopamine release.

To test this hypothesis, medically stable untreated adult MDD outpatients were enrolled to have different levels of inflammation (as defined by plasma C-reactive protein) while establishing a platform to investigate the involvement of potential therapeutic targets in patients with increased inflammation. [CRP] levels) was studied in two visits involving an acute challenge with the dopamine precursor levodopa (L-DOPA; 250 mg) and placebo (double-blind, randomized order ∼1-week apart).

Resting-state (rs) FC in the classical ventral striatum to ventromedial prefrontal cortex reward circuit was calculated using a targeted, a priori approach.

Data are available at pre- and post-test (n= 31/40) stability of rsFC was based on visits and CRP > 2 mg/L was defined as the cutoff point for patients showing positive FC responses (before pretreatment) to L-DOPA versus placebo.Page<0.01)

Elevated post-L-DOPA FC CRP >2 mg/L was confirmed in all patients (n= 40) where the rsFC data after testing (b= 0.15, Page= 0.006), and task-based (tb) FC with reward anticipation (b= 0.15, Page= 0.013).

While out-of-scanner effort-based motivation was positively associated with rsFC independent of treatment or CRP, anhedonia scores were negatively associated with rsFC only in patients with CRP > 2 mg/L after L-DOPA.R= -0.56, Page= 0.012).

FC needs to be further validated in larger samples as a biomarker for targeted therapies, including dopaminergic agents, with increased inflammation in reward circuits in MDD patients.

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