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Saturday, November 26, 2022

When severe infection causes long-term mood disorders: a promising approach to preventing mental illness after a transient infection

The brain is able to detect and control localized or systemic inflammation using two communication pathways. The first, humoral, uses specific brain structures that enable circulating inflammatory mediators to enter the brain. The second, neuralgia, includes the nerves whose sensory afferents transmit the locally detected inflammatory signal.

The vagus nerve therefore uses the receptors identified to detect digestion or inflammation of the lungs. Specific brain structures and networks sense and integrate these humoral and neural messages and modulate a regulatory response involving neuroendocrine, neurovegetative and behavioral elements. These corrective interventions are controlled by the hypothalamus and hypophysis – the autonomic nervous system and limbic system, respectively. Neuroendocrine activation is characterized by the release of the main stress hormone cortisol. The autonomic response involves the combined activation of the sympathetic and vagal systems, the latter believed to induce a local anti-inflammatory response. Behavioral changes affect mood, attention, sleep and appetite. The overall response is aimed at controlling inflammation so as to preserve physiological integrity, or homeostasis. But in some circumstances, it can be adapted incorrectly and lead to immunological and/or psychological disorders.

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A severe infection known as sepsis is the most common condition capable of inducing this defense strategy against inflammatory stress. Sepsis is the leading cause of death worldwide and represents a major public health challenge. What makes the situation worse is that sepsis is also associated with chronic psychiatric disorders such as anxiety, depression and post-traumatic stress disorder. These conditions significantly increase the risk of suicide and have lasting effects on the personal, social and professional lives of patients. Professor Tarek Sharcher, Head of the Department of Saint-Anne Neurology, explains, “So far no preventive treatment has been demonstrated to be effective, probably due to a lack of understanding of the pathophysiology of these disorders, particularly neural networks in their onset. are trapped.” ,

In an experimental study published in the journal mind, a team of scientists from the Institut Pasteur (Perception and Memory Laboratory) and clinicians from the Paris Psychiatry and Neurosciences University Hospital Group (GHU) (Department of Neurological Resuscitation) used pharmacogenetic techniques to identify a dedicated neural circuit, in which the amygdala contains the central nucleus. and the bed nucleus of the stria terminalis. Activation of this circuit in the first few hours after sepsis induces anxious behavior two weeks after the infection has cleared. This behavior observed in rats mimics post-traumatic stress disorder observed in patients recovering from sepsis.

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“This discovery paves the way for new therapeutic strategies for sepsis: we observed that administering an agent capable of inhibiting the hyperactivity of this circuit reduces the risk of developing anxiety disorders,” said Professor Pierre-Marie Ledo, Institute Pasteur and CNRS point out. This effect is thought to be partly associated with reduced activation of the vagal afferent integration center.

This study is of particular interest because it identifies a dedicated circuit for both post-sepsis anxiety and potential pharmacological treatments. The latter will soon be tested in a multicentre randomized clinical trial. By highlighting the link between neuroinflammation and mental disorders, this research resonates with the current context of the COVID-19 pandemic and the protracted COVID-19 pandemic.

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material provided by Institute Pasteur, Note: Content can be edited for style and length.

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