Involvement of Nuclear Factor-κB in Inflammation and Neuronal Plasticity Associated with Post-Traumatic Stress Disorder

Abstract

Post-traumatic stress disorder (PTSD) is a debilitating psychiatric condition which develops either due to stress or witnessing a traumatic situation. PTSD is characterized by acute and chronic stress response exhibit anxiety, fear, and an increased inflammatory etiology. Inflammation contributes a critical role in several parts of the brain that control fear and flashback cognatic function. It is known that impairment of the neurological circuit leads to the development of PTSD. Evidence has suggested that dysregulation of the sympathetic nervous system and hypothalamic-pituitary adrenal (HPA) axis and inflammatory responsiveness are pivotal and a greater risk in PTSD. NF-κB, a master regulator for inflammation, has been showed to modulate memory reconsolidation and synaptic plasticity; however, NF-κB’s association with PTSD remain elusive. In this review, we provide relevant findings regarding NF-κB activity in various components of brain and describe a potential mechanism linking PTSD using preclinical and clinical models. We envisage NF-κB signaling as a crucial mediator for inflammation, cognitive function, memory restoration and behavioral actions of stress and suggest that it could be used for therapeutic intervention in PTSD.

Corticosterone enhances formation of non-fear but not fear memory during infectious illness

“…It is possible that in our study we observed a “ceiling effect” considering the high efficacy of our fear conditioning regiment in both corticosterone-treated and untreated groups. This potential “ceiling effect” could also be a product of the high endogenous catecholamine and glucocorticoid levels as well as the inflammatory response to the illness ( Gupta and Guleria, 2022 ). The results suggest that, in the setting of this neuroendocrine and inflammatory background, supplemental glucocorticoids do not have a significant modulatory effect on the development of fear memory.…”

Modulation of redox-sensitive transcription factors with polyphenols as pathogenetically grounded approach in therapy of systemic inflammatory response

“…Numerous reports have emphasized an important role of NFκB in the pathogenesis of various diseases that, on the one hand, are followed with the LGSIP development, e. g. metabolic syndrome [ 65 , 66 ], atherosclerosis [ 67 ], diabetes mellitus type 2 [ 68 ], osteoporosis [ 69 ], rheumatoid arthritis [ 70 ], inflammatory bowel diseases [ 71 ], multiple sclerosis and autoimmune encephalomyelitis [ 72 ], asthma and chronic obstructive pulmonary disease [ 73 ], periodontal disease [ 62 ], post-traumatic stress disorder [ 74 ], etc. But on the other, researchers point out a role of the NFκB activation in the mechanisms of diseases followed by the HGSIP development, in particular, septic shock [ 75 ], DIC [ 76 ], traumatic brain injury [ 77 ], burn injury [ 78 ], cytokine storming under COVID-19 [ 79 ].…”

Особливості Фармакологічної Корекції Соматичних Проявів Депресії Та Когнітивного Зниження У Хворих Із Тривожно-Депресивними Розладами У Воєнний Час

“…Когнітивний дефіцит при ВДР є відновлюваним, неспецифічним і клінічно значущим; відхилення стосуються сфер навчання, пам'яті, виконавчих функцій, уваги, концентрації та швидкості обробки інформації [7,8]. Вважають, що порушення соціального пізнання при ПТСР зумовлено функціональними змінами у структурі головного мозку: ушкодженням фронтолімбічної зони та мигдалини, яке призводить до порушення фронтальної регуляції «згори донизу», а запальний процес, що провокується NF-κВ, гальмує нейропластичність, посилює когнітивну дисфункцію, утруднює процеси відновлення пам'яті та рефлекторні дії під час стресу [9,10].…”