Neuroinflammation and depression: A review

Abstract

Some recent clinical and preclinical evidence suggests that neuroinflammation is a key factor that interacts with the three neurobiological correlates of major depressive disorder: depletion of brain serotonin, dysregulation of the hypothalamus-pituitaryadrenal (HPA) axis and alteration of the continuous production of adult-generated

To stress or not to stress: Brain-behavior-immune interaction may weaken or promote the immune response to SARS-CoV-2

“…This boosts for example vaccine responses and post-operative recovery but can also contribute to the fatal effects of a cytokine storm ( Kempuraj et al, 2020 ). Moreover, psychological states that are associated with repeatedly high stress states such as depression or PTSD are also associated with a chronic low-grade increase of these cytokines ( Speer et al, 2018 ; Troubat et al, 2020 ). Vice versa, cytokines produced in response to an inflammatory challenge can affect the HPA, closing a vicious cycle ( Straub et al, 2011 ).…”

Depression in focus: Insights from animal and human data, from molecular to behavioural analyses

“…The relation between inflammation and depression has been a topic of increased interest since the late 1990s, following evidence that immune challenges can induce depressive-like "sickness behaviour" and that rapid onset of MDD can be an adverse effect of interferon therapy. After presenting the main players of brain immunity, Troubat et al (2020) discussed how neuroinflammation interacts with three neurobiological correlates of MDD: monoamine depletion, the endocrine hypothalamus-pituitary-adrenal (HPA) axis and neurogenesis. A research article from Nothdurfter et al (2019) further showed in depressed patients that the pro-inflammatory cytokine interleukin 17 might be a biomarker of treatment resistance in MDD.…”

“…After presenting the main players of brain immunity, Troubat et al. (2020) discussed how neuroinflammation interacts with three neurobiological correlates of MDD: monoamine depletion, the endocrine hypothalamus–pituitary–adrenal (HPA) axis and neurogenesis. A research article from Nothdurfter et al.…”

Crosstalk Between ATP-P2X7 and Adenosine A2A Receptors Controlling Neuroinflammation in Rats Subject to Repeated Restraint Stress

“…Depression represents the major burden of disease in Europe (Andlin-Sobocki et al, 2005) and the constellation of mood alterations associated with depression can be recapitulated in animal models repeatedly exposed to different stressors (de Kloet et al, 2005;Berton et al, 2012). The use of animal models converges with imaging studies to identify modifications of different brain regions, such as the hippocampus, prefrontal, and limbic cortices, that are associated with mood dysfunction (de Kloet et al, 2005) and provide compelling evidence for the involvement of neuroinflammation (Rial et al, 2016;Deng et al, 2020;Troubat et al, 2021) and of synaptic dysfunction (Duman and Aghajanian, 2012;Vose and Stanton, 2017) as key processes in the etiology of major depression. However, the identification of molecular systems that may be targeted to correct depressive symptoms has still failed to yield novel and effective anti-depressants (Ménard et al, 2016).…”