scholarly journals Effects of Acute Exercise on Circulating Soluble Form of the Urokinase Receptor in Patients With Major Depressive Disorder

2017 ◽  
Vol 12 ◽  
pp. 117727191770419 ◽  
Author(s):  
Anna Gustafsson ◽  
Filip Ventorp ◽  
Anita GM Wisén ◽  
Lars Ohlsson ◽  
Lennart Ljunggren ◽  
...  

Inflammation has been proposed to play a role in the generation of depressive symptoms. Previously, we demonstrated that patients with major depressive disorder (MDD) have increased plasma levels of the soluble form of the urokinase receptor (suPAR), a marker for low-grade inflammation. The aim of this study was to test the hypothesis that acute exercise would induce inflammatory response characterized by increased suPAR and elucidate whether patients with MDD display altered levels of suPAR in response to acute exercise. A total of 17 patients with MDD and 17 controls were subjected to an exercise challenge. Plasma suPAR (P-suPAR) was analyzed before, during, and after exercise. There was a significantly higher baseline P-suPAR in the patients with MDD, and the dynamic changes of P-suPAR during the exercise were significantly lower in the patients with MDD, compared with the controls. This study supports the hypothesis that an activation of systemic inflammatory processes, measured as elevated P-suPAR, is involved in the pathophysiology of depression. The study concludes that P-suPAR is influenced by acute exercise, most likely due to release from activated neutrophils.

Physiology ◽  
2019 ◽  
Vol 34 (2) ◽  
pp. 123-133 ◽  
Author(s):  
Kenny L. Chan ◽  
Flurin Cathomas ◽  
Scott J. Russo

Metabolic syndrome and major depression are two of the most common and debilitating disorders worldwide, occurring with significant rates of comorbidity. Recent studies have uncovered that each of these conditions is associated with chronic, low-grade inflammation. This is characterized by increased circulating pro-inflammatory cytokines, altered leukocyte population frequencies in blood, accumulation of immune cells in tissues including the brain, and activation of these immune cells. Cytokines that become elevated during obesity can contribute to the progression of metabolic syndrome by directly causing insulin resistance. During chronic stress, there is evidence that these cytokines promote depression-like behavior by disrupting neurotransmitter synthesis and signal transduction. Animal models of obesity and depression have revealed a bi-directional relationship whereby high-fat feeding and chronic stress synergize and exacerbate metabolic dysregulation and behavioral abnormalities. Although far from conclusive, emerging evidence suggests that inflammation in the central and peripheral immune system may link metabolic syndrome to major depressive disorder. In this review, we will synthesize available data supporting this view and identify critical areas for future investigation.


2021 ◽  
Vol 11 (8) ◽  
pp. 110
Author(s):  
Cristina Peña-Vargas ◽  
Guillermo Armaiz-Peña ◽  
Eida Castro-Figueroa

According to the field of affective neuroscience, grief has been identified as one of the seven primary emotions necessary for human survival. However, maladaptive grief could cause significant impairment in an individual’s life, leading to psychopathologies such as major depressive disorder. Research on grief has shifted to a biopsychosocial approach, leaving behind outdated models—such as the Kübler-Ross theory—that have shown poor consistency. The field of psychoneuroimmunology has identified adverse life events such as social loss as being associated with major depressive disorder, and inflammatory processes in chronic health conditions. Likewise, scientists in the field of affective neuroscience have theorized that prolonged and sustained activation of the grief neurological pathway can cause a cascade of neurotransmitters that inhibits the reward-seeking system, causing symptoms of depression. The objective of this review is to highlight findings on the grief process using a biopsychosocial approach to explore grief’s impact on psychopathophysiology.


Sign in / Sign up

Export Citation Format

Share Document