TY - JOUR
T1 - Emphasizing the Crosstalk Between Inflammatory and Neural Signaling in Post-traumatic Stress Disorder (PTSD)
AU - Govindula, Anusha
AU - Ranadive, Niraja
AU - Nampoothiri, Madhavan
AU - Rao, C. Mallikarjuna
AU - Arora, Devinder
AU - Mudgal, Jayesh
N1 - Funding Information:
The authors wish to acknowledge the infrastructural support provided by the Department of Pharmacology, Manipal College of Pharmaceutical Sciences, and Manipal Academy of Higher Education, Manipal-576104, India. The authors also would like to thank the Department of Science and Technology (DST), New Delhi, India for appointing AG under the Women Scientist-A (WOS-A) scheme (DST/WOS-A/LS-37/2021). The authors are grateful to the developers of Inkscape version 1.2 ( https://inkscape.org/ ) free version which was used for the development of the images in the manuscript except Fig. 3 (created by using Microsoft PowerPoint 2019).
Publisher Copyright:
© 2023, The Author(s).
PY - 2023
Y1 - 2023
N2 - Post-traumatic stress disorder (PTSD) is a chronic incapacitating condition with recurrent experience of trauma-related memories, negative mood, altered cognition, and hypervigilance. Agglomeration of preclinical and clinical evidence in recent years specified that alterations in neural networks favor certain characteristics of PTSD. Besides the disruption of hypothalamus-pituitary-axis (HPA) axis, intensified immune status with elevated pro-inflammatory cytokines and arachidonic metabolites of COX-2 such as PGE2 creates a putative scenario in worsening the neurobehavioral facet of PTSD. This review aims to link the Diagnostic and Statistical Manual of mental disorders (DSM-V) symptomology to major neural mechanisms that are supposed to underpin the transition from acute stress reactions to the development of PTSD. Also, to demonstrate how these intertwined processes can be applied to probable early intervention strategies followed by a description of the evidence supporting the proposed mechanisms. Hence in this review, several neural network mechanisms were postulated concerning the HPA axis, COX-2, PGE2, NLRP3, and sirtuins to unravel possible complex neuroinflammatory mechanisms that are obscured in PTSD condition.
AB - Post-traumatic stress disorder (PTSD) is a chronic incapacitating condition with recurrent experience of trauma-related memories, negative mood, altered cognition, and hypervigilance. Agglomeration of preclinical and clinical evidence in recent years specified that alterations in neural networks favor certain characteristics of PTSD. Besides the disruption of hypothalamus-pituitary-axis (HPA) axis, intensified immune status with elevated pro-inflammatory cytokines and arachidonic metabolites of COX-2 such as PGE2 creates a putative scenario in worsening the neurobehavioral facet of PTSD. This review aims to link the Diagnostic and Statistical Manual of mental disorders (DSM-V) symptomology to major neural mechanisms that are supposed to underpin the transition from acute stress reactions to the development of PTSD. Also, to demonstrate how these intertwined processes can be applied to probable early intervention strategies followed by a description of the evidence supporting the proposed mechanisms. Hence in this review, several neural network mechanisms were postulated concerning the HPA axis, COX-2, PGE2, NLRP3, and sirtuins to unravel possible complex neuroinflammatory mechanisms that are obscured in PTSD condition.
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U2 - 10.1007/s11481-023-10064-z
DO - 10.1007/s11481-023-10064-z
M3 - Review article
AN - SCOPUS:85153344018
SN - 1557-1890
JO - Journal of NeuroImmune Pharmacology
JF - Journal of NeuroImmune Pharmacology
ER -