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REVIEW ARTICLE

Post-traumatic stress disorder: Cerebral and extracerebral processing of traumatic memories and treatment strategies

Adonis Sfera1,2,3 ,  Jacob J. Anton4 ,  Jasper H. C. Luong5 ,  Zisis Kozlakidis6*
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1 Patton State Hospital, Patton, CA, United States of America
2 Department of Psychiatry, University of California Riverside, Riverside, CA, United States of America
3 Department of Psychiatry, Loma Linda University, Loma Linda, CA, United States of America
4 Department of Health Sciences, California Baptist University, Riverside, CA, United States of America
5 Smoke-Free and Healthy Life Association of Macau, Macau SAR, China
6 International Agency for Research on Cancer, World Health Organization, Lyon, Rhone Alpes, France
Global Translational Medicine, 3974 https://doi.org/10.36922/gtm.3974
Submitted: 19 June 2024 | Accepted: 18 September 2024 | Published: 22 November 2024
© 2024 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
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Abstract

Post-traumatic stress disorder (PTSD) is a severe neuropsychiatric condition characterized by anxiety-related symptoms, including intrusive memories. However, the exact anatomic location of traumatic memories remains unclear. Traumatic imagery may involve the amygdala and posterior cingulate cortex, rather than the hippocampus. Besides the central nervous system, cells and even proteins can process information and store memories. For instance, >36% of cardiac transplant recipients inherit donor personality traits, emphasizing that tissues can store and recall memories. Moreover, physical therapists mention “musculofascial memories,” that is, the ability of muscles and fascia to retain the memory of past injuries and adapt their function accordingly. Immune cells record previous infections, demonstrating the broader perspective of memory storage in the body. At the cellular level, psychological stress induces premature cellular senescence, a survival program characterized by proliferation arrest; resistance to apoptosis; and a toxic secretome known as the senescence-associated secretory phenotype (SASP). SASP contains brain-derived neurotropic factor (BDNF), a neurotrophin linked to fear memory that is frequently elevated in the peripheral blood of patients with PTSD. Endothelial cells (ECs), the tiles paving the lumen of large and small vessels, age earlier than other cells in patients with severe mental illness, including PTSD. Senescent ECs release SASP directly into the systemic circulation, spreading senescence throughout the body. In this narrative review, we hypothesize that ECs store traumatic memories and SASP-associated BDNF activates traumatic imagery. We also discuss membrane lipid replacement, mitochondrial transplantation and transfer, and several natural and synthetic compounds that may counteract endothelial senescence and SASP.

Graphical abstract
Keywords
PTSD
Psychological trauma
Traumatic amnesia
Traumatic hypermnesia
Cellular senescence
Funding
None.
Conflict of interest
The authors declare that they have no competing interests.
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Global Translational Medicine, Electronic ISSN: 2811-0021 Print ISSN: 3060-8600, Published by AccScience Publishing
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