Depression is a mental disorder that affects millions of people worldwide. According to the World Health Organization, depression is the leading cause of disability globally. Moreover, its prevalence has increased significantly in the last few decades. The global threat and prevalence of depression can be attributed to various factors, including genetic predisposition, environmental factors, and lifestyle choices. In addition, the stigma surrounding mental illness can prevent people from seeking help and getting proper treatment.
Neurotransmitters, a kind of brain chemical that transmits signals between nerve cells, play an important role in brain function. For example, several neurotransmitters are involved in depression, including serotonin, norepinephrine, and dopamine.
Serotonin is often referred to as the “feel-good” neurotransmitter and is involved in regulating mood, appetite, and sleep. Norepinephrine is responsible for the body’s “fight or flight” response and regulates attention, alertness, and arousal. Dopamine is involved in regulating motivation, reward, and pleasure.
The role of these neurotransmitters in depression is complex and not fully understood. However, research suggests that imbalances in these neurotransmitters may play a role in the development of depression. For example, low serotonin levels are associated with depressive symptoms, and drugs that increase serotonin levels in the brain are often used to treat depression.
In recent years, there has been increasing evidence regarding the role of brain inflammation in depression. Inflammation is the body’s natural response to injury or infection. However, chronic inflammation can contribute to the development of various diseases, including depression. Studies have shown that people with depression have increased inflammatory markers in their blood and cerebrospinal fluid levels.
One theory is that inflammation in the brain can disrupt the balance of neurotransmitters and contribute to the development of depression. In addition, inflammation can affect the functioning of the hypothalamic-pituitary-adrenal (HPA) axis, which regulates the body’s response to stress. Dysregulation of the HPA axis has been implicated in the development of depression.
Furthermore, chronic stress can lead to an overactive immune response and chronic inflammation. This, in turn, can lead to a decrease in the production of neurotrophic factors, which are involved in promoting the growth and survival of neurons. A decrease in neurotrophic factors can contribute to the development of depression by impairing the functioning of neural circuits involved in mood regulation.
A drug that increases dopamine levels in the brain may also help reduce brain inflammation and depression
One of the factors that contribute to depression is inflammation. Inflammation is a natural response of the body to injury or infection. However, chronic inflammation can contribute to the development of depression. Previous studies have shown that inflammation in the brain can affect the synthesis and release of dopamine. This neurotransmitter is involved in regulating mood, reward, and pleasure.
To test the hypothesis that inflammation affects the dopamine system in the brain, researchers conducted a study on patients living with major depressive disorder (MDD). The participants were classified according to their levels of inflammation as indicated by their plasma C-reactive protein (CRP) levels. They were then given an acute challenge with the dopamine precursor levodopa (L-DOPA) and a placebo in a double-blind, randomized order about one week apart.
The study’s primary outcome was resting-state functional connectivity (rsFC) in a specific reward circuit in the brain. In addition, the researchers found that patients with CRP levels higher than 2 mg/L who were given L-DOPA showed a positive rsFC response compared to those who were given the placebo. This suggests that L-DOPA can improve the connectivity in the brain’s reward circuit, which may help alleviate depressive symptoms in patients with increased inflammation.
The study also found that the change in anhedonia scores, a symptom of depression characterized by the inability to feel pleasure, was negatively correlated with rsFC after L-DOPA only in patients with CRP levels higher than 2 mg/L. This suggests that L-DOPA may help improve the symptoms of anhedonia in patients with increased inflammation.
In conclusion, this study suggests that inflammation can affect the dopamine system in the brain, which can contribute to the development of depression. Therefore, the results of this study indicate that L-DOPA may be a potential treatment for depression in patients with increased inflammation.
