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Analysis of the data revealed a link between inflammation and depression
Depression is a common mental disorder, the effective treatment of which remains a challenging problem worldwide. The mechanism of depression development has been studied in sufficient depth to formulate various hypotheses. Prominent among them is the monoamine neurotransmitter hypothesis, but it has significant limitations, as more than one-third of patients do not respond to traditional treatments aimed at disrupting monoamine transmission.
Research over the past several decades has increasingly pointed to the link between inflammation and depression as a potential key factor in the pathophysiology of depression
In a study recently published in the journal Brain, Behavior, and Immunity, lead author Jonas Hagenberg and scientists from the Medical Genomics Project Group focused more attention on the link between depression and inflammation and other factors. They measured more than 40 immune markers in the blood of 237 participants.
This was a transdiagnostic study, meaning the scientists included not only patients with depression, but also those with other disorders such as anxiety or substance use.
During the study, biological data was collected from the participants. About one-third of patients with depressive symptoms already had elevated levels of inflammation. However, inflammation was often only detected using very simple and non-specific indicators.
To better understand the link between depression and the immune system, the researchers measured a large number of different biological factors and found some patterns.
In addition to immune markers, the scientists measured the activity of more than 12,000 different genes in immune cells, as well as the severity of depressive symptoms. They also took into account the body mass index (BMI) and age of the participants, as both of these factors influence inflammation. Using machine learning techniques, the researchers tried to recognize patterns in the findings.
The team identified four groups of participants. In addition to C-reactive protein (CRP), a standard marker used to measure inflammation, the immune markers interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and several chemokines (a class of immune markers) helped in differentiating these groups.
The largest group included 121 participants – they had fewer depressive symptoms, low levels of inflammation and tended to be younger. The next two groups consisted of 77 participants who were characterized by high levels of depressive symptoms, high levels of inflammation, and higher body mass index. The last group consisted of 39 participants with high levels of depressive symptoms but low levels of inflammation.
The levels of gene activity differed mainly between the group that contained patients with fewer symptoms and the other three groups, which had more severe symptoms. Interestingly, some depression-related genes were also linked to certain immune cells, suggesting that some types of immune cells may be more important in depression than others.
“Our results show that while CRP is a good marker, there are others that may be useful and require further research – such as IL-1RA and chemokines,” explains Hagenberg. “In addition, the association between severity of depressive symptoms, inflammatory markers and BMI shows that depression needs to be treated holistically – this is not a new result, but it further emphasizes the importance of body weight.”
The inclusion of data beyond the CRP score allows researchers to further understand the link between the immune system and depression. These findings may help develop more individualized and precise treatments for subgroups of depressed patients in the future.
This study expands the understanding of specific aspects of the use of anti-inflammatory strategies to treat depression, laying the groundwork for the development of precision medicine for people suffering from “inflammatory” depression.
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