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Metabolic Regulators of Psychological Stress and Brain Trauma

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 3423

Special Issue Editor


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Guest Editor
Medical Readiness Systems Biology, Walter Reed Army Institute of Research, Silver Spring, MD 20910, USA
Interests: epigenetics; transcriptomics; gene regulation; comparative genomics; bioinformatics and computational biology

Special Issue Information

Dear Colleagues,

Small molecules or metabolites comprise a wide chemical library, including short-chain fatty acids (e.g., acetate, butyrate, etc.); bio-energy cycle products (e.g., ATP, AMP, pyruvate, lactate, etc.); microbial fermentation products (e.g., formate, succinate, etc.); lipids (e.g. choline, betaine etc.); bile acids (e.g. lithocholate, glycocholate, etc.); amino acids and polyamine; phenolic compounds (e.g. phenylacetate, benzoic acid, etc.); indolic compounds (e.g. indole, indoxyl sulfate, etc.); hormones, their precursors and derivatives (e.g. GABA, serotonin, etc.), and xenobiotics. The majority of these metabolites are the end products of biological functions; hence, systematic interrogation of the metabolite profiles can inform the longitudinal endophenotypes of disease. For instance, temporal monitoring of neuro-endocrines or energy-cycle products can score the severity of the past occurrences of immune dysfunction or energy deficiency, respectively; subsequent trend analysis can forecast the chances of disease relapse or eradication. In recent years, this knowledge has been used to explain the pathophysiology of several psychological diseases and brain trauma, which embodies the focus of this Special Issue.

We welcome original articles and review works on the following subjects:

(a)  The role of metabolites and their associations with other omics, such genome, epigenome and metagenome to explain the endophenotype triggered by psychological stress and brain trauma.

(b) Chemical biomarker studies and relevant molecular underpinnings that are associated with psychological stress, brain trauma and its comorbidities.   

Dr. Rasha Hammamieh
Guest Editor

Manuscript Submission Information

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Keywords

  • small molecules and chemicals
  • metabolomics, lipidomics, and their interdependence to other omics, such as transcriptomics, epigenomics, proteomics, metagenomics etc.
  • metabolites and their endophenotypes
  • neuro-endocrine systems
  • biological networks and their regulators
  • psychological stress and comorbidities
  • disease biology and dynamics
  • therapeutic targets
  • biomarkers

Published Papers (2 papers)

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Research

18 pages, 12656 KiB  
Article
Neuroinflammation Profiling of Brain Cytokines Following Repeated Blast Exposure
by Lanier Heyburn, Andrew Batuure, Donna Wilder, Joseph Long and Venkatasivasai Sujith Sajja
Int. J. Mol. Sci. 2023, 24(16), 12564; https://doi.org/10.3390/ijms241612564 - 8 Aug 2023
Cited by 3 | Viewed by 1045
Abstract
Due to use of explosive devices and heavy weapons systems in modern conflicts, the effect of BW on the brain and body is of increasing concern. These exposures have been commonly linked with neurodegenerative diseases and psychiatric disorders in veteran populations. A likely [...] Read more.
Due to use of explosive devices and heavy weapons systems in modern conflicts, the effect of BW on the brain and body is of increasing concern. These exposures have been commonly linked with neurodegenerative diseases and psychiatric disorders in veteran populations. A likely neurobiological link between exposure to blasts and the development of neurobehavioral disorders, such as depression and PTSD, could be neuroinflammation triggered by the blast wave. In this study, we exposed rats to single or repeated BW (up to four exposures—one per day) at varied intensities (13, 16, and 19 psi) to mimic the types of blast exposures that service members may experience in training and combat. We then measured a panel of neuroinflammatory markers in the brain tissue with a multiplex cytokine/chemokine assay to understand the pathophysiological process(es) associated with single and repeated blast exposures. We found that single and repeated blast exposures promoted neuroinflammatory changes in the brain that are similar to those characterized in several neurological disorders; these effects were most robust after 13 and 16 psi single and repeated blast exposures, and they exceeded those recorded after 19 psi repeated blast exposures. Tumor necrosis factor-alpha and IL-10 were changed by 13 and 16 psi single and repeated blast exposures. In conclusion, based upon the growing prominence of negative psychological health outcomes in veterans and soldiers with a history of blast exposures, identifying the molecular etiology of these disorders, such as blast-induced neuroinflammation, is necessary for rationally establishing countermeasures and treatment regimens. Full article
(This article belongs to the Special Issue Metabolic Regulators of Psychological Stress and Brain Trauma)
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15 pages, 2132 KiB  
Article
The Genetic Basis for the Increased Prevalence of Metabolic Syndrome among Post-Traumatic Stress Disorder Patients
by Burook Misganaw, Ruoting Yang, Aarti Gautam, Seid Muhie, Synthia H. Mellon, Owen M. Wolkowitz, Kerry J. Ressler, Francis J. Doyle III, Charles R. Marmar, Marti Jett and Rasha Hammamieh
Int. J. Mol. Sci. 2022, 23(20), 12504; https://doi.org/10.3390/ijms232012504 - 19 Oct 2022
Cited by 3 | Viewed by 1867
Abstract
Post-traumatic stress disorder (PTSD) is a highly debilitating psychiatric disorder that can be triggered by exposure to extreme trauma. Even if PTSD is primarily a psychiatric condition, it is also characterized by adverse somatic comorbidities. One illness commonly co-occurring with PTSD is Metabolic [...] Read more.
Post-traumatic stress disorder (PTSD) is a highly debilitating psychiatric disorder that can be triggered by exposure to extreme trauma. Even if PTSD is primarily a psychiatric condition, it is also characterized by adverse somatic comorbidities. One illness commonly co-occurring with PTSD is Metabolic syndrome (MetS), which is defined by a set of health risk/resilience factors including obesity, elevated blood pressure, lower high-density lipoprotein cholesterol, higher low-density lipoprotein cholesterol, higher triglycerides, higher fasting blood glucose and insulin resistance. Here, phenotypic association between PTSD and components of MetS are tested on a military veteran cohort comprising chronic PTSD presentation (n = 310, 47% cases, 83% male). Consistent with previous observations, we found significant phenotypic correlation between the various components of MetS and PTSD severity scores. To examine if this observed symptom correlations stem from a shared genetic background, we conducted genetic correlation analysis using summary statistics data from large-scale genetic studies. Our results show robust positive genetic correlation between PTSD and MetS (rg[SE] = 0.33 [0.056], p = 4.74E-09), and obesity-related components of MetS (rg = 0.25, SE = 0.05, p = 6.4E-08). Prioritizing genomic regions with larger local genetic correlation implicate three significant loci. Overall, these findings show significant genetic overlap between PTSD and MetS, which may in part account for the markedly increased occurrence of MetS among PTSD patients. Full article
(This article belongs to the Special Issue Metabolic Regulators of Psychological Stress and Brain Trauma)
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