한빛사논문
Ja Wook Koo1,2, Eric S. Wohleb3,*
1Department of Neural Development and Disease, Korea Brain Research Institute, Daegu, Korea
2Department of Brain and Cognitive Sciences, Daegu Gyeongbuk Institute of Science and Technology (DGIST), Daegu, Korea
3Department of Pharmacology & Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America
*Corresponding author
Abstract
Chronic stress causes physiological and hormonal adaptations that lead to neurobiological consequences and behavioral and cognitive impairments. In particular, chronic stress is shown to drive reduced neurogenesis and altered synaptic plasticity in brain regions that regulate mood and motivation. The neurobiological and behavioral effects of stress resemble pathophysiology and symptoms observed in psychiatric disorders, suggesting that there are similar mechanisms.
Accumulating evidence indicates that neuroimmune systems, particularly microglia, have a critical role in regulating the neurobiology of stress. Preclinical models indicate that chronic stress provokes changes in microglia phenotype and increases inflammatory cytokine signaling that affect neuronal function, leading to synaptic plasticity deficits and impaired neurogenesis. More recent work shows that microglia can also phagocytose neuronal elements and contribute to structural remodeling of neurons in response to chronic stress.
In this review we intend to highlight work by the Duman research group (as well as others) that revealed how chronic stress shapes neuroimmune function and, in turn, how inflammatory mediators and microglia contribute to the neurobiological effects of chronic stress. We will also provide considerations to engage neuroimmune systems and improve treatment for psychiatric disorders.
Clinical and preclinical evidence linking chronic stress, neuroimmune dysregulation, and psychiatric disorders
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