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Lower amygdala fatty acid amide hydrolase in violent offenders with antisocial personality disorder: an [(11)C]CURB positron emission tomography study
Antisocial personality disorder (ASPD) imposes a high societal burden given the repetitive reactive aggression that affected individuals perpetrate. Since the brain endocannabinoid system (ECS) has been implicated in ASPD and aggressive behavior, we utilized [(11)C]CURB positron emission tomography...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7814116/ https://www.ncbi.nlm.nih.gov/pubmed/33462180 http://dx.doi.org/10.1038/s41398-020-01144-2 |
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author | Kolla, Nathan J. Boileau, Isabelle Karas, Karolina Watts, Jeremy J. Rusjan, Pablo Houle, Sylvain Mizrahi, Romina |
author_facet | Kolla, Nathan J. Boileau, Isabelle Karas, Karolina Watts, Jeremy J. Rusjan, Pablo Houle, Sylvain Mizrahi, Romina |
author_sort | Kolla, Nathan J. |
collection | PubMed |
description | Antisocial personality disorder (ASPD) imposes a high societal burden given the repetitive reactive aggression that affected individuals perpetrate. Since the brain endocannabinoid system (ECS) has been implicated in ASPD and aggressive behavior, we utilized [(11)C]CURB positron emission tomography to investigate fatty acid amide hydrolase (FAAH), an enzyme of the ECS that degrades anandamide, in 16 individuals with ASPD and 16 control participants. We hypothesized that FAAH density would be lower in the amygdala for several reasons. First, decreased FAAH expression is associated with increased cannabinoid receptor 1 stimulation, which may be responsible for amygdala hyper-reactivity in reactive aggression. Second, the amygdala is the seat of the neural circuit mediating reactive aggression. Third, other PET studies of externalizing populations show reduced brain FAAH density. Conversely, we hypothesized that FAAH expression would be greater in the orbitofrontal cortex. Consistent with our hypothesis, we found that amygdala FAAH density was lower in the amygdala of ASPD (p = 0.013). Cerebellar and striatal FAAH expression were inversely related with impulsivity (cerebellum: r = −0.60, p = 0.017; dorsal caudate: r = −0.58, p = 0.023; dorsal putamen: r = −0.55, p = 0.034), while cerebellar FAAH density was also negatively associated with assaultive aggression (r = −0.54, p = 0.035). ASPD presents high levels of disruptive behavior with few, if any, efficacious treatment options. Novel therapeutics that increase FAAH brain levels in a region-specific manner could hold promise for attenuating certain symptom clusters of ASPD, although our results require replication. |
format | Online Article Text |
id | pubmed-7814116 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-78141162021-01-25 Lower amygdala fatty acid amide hydrolase in violent offenders with antisocial personality disorder: an [(11)C]CURB positron emission tomography study Kolla, Nathan J. Boileau, Isabelle Karas, Karolina Watts, Jeremy J. Rusjan, Pablo Houle, Sylvain Mizrahi, Romina Transl Psychiatry Article Antisocial personality disorder (ASPD) imposes a high societal burden given the repetitive reactive aggression that affected individuals perpetrate. Since the brain endocannabinoid system (ECS) has been implicated in ASPD and aggressive behavior, we utilized [(11)C]CURB positron emission tomography to investigate fatty acid amide hydrolase (FAAH), an enzyme of the ECS that degrades anandamide, in 16 individuals with ASPD and 16 control participants. We hypothesized that FAAH density would be lower in the amygdala for several reasons. First, decreased FAAH expression is associated with increased cannabinoid receptor 1 stimulation, which may be responsible for amygdala hyper-reactivity in reactive aggression. Second, the amygdala is the seat of the neural circuit mediating reactive aggression. Third, other PET studies of externalizing populations show reduced brain FAAH density. Conversely, we hypothesized that FAAH expression would be greater in the orbitofrontal cortex. Consistent with our hypothesis, we found that amygdala FAAH density was lower in the amygdala of ASPD (p = 0.013). Cerebellar and striatal FAAH expression were inversely related with impulsivity (cerebellum: r = −0.60, p = 0.017; dorsal caudate: r = −0.58, p = 0.023; dorsal putamen: r = −0.55, p = 0.034), while cerebellar FAAH density was also negatively associated with assaultive aggression (r = −0.54, p = 0.035). ASPD presents high levels of disruptive behavior with few, if any, efficacious treatment options. Novel therapeutics that increase FAAH brain levels in a region-specific manner could hold promise for attenuating certain symptom clusters of ASPD, although our results require replication. Nature Publishing Group UK 2021-01-18 /pmc/articles/PMC7814116/ /pubmed/33462180 http://dx.doi.org/10.1038/s41398-020-01144-2 Text en © The Author(s) 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Kolla, Nathan J. Boileau, Isabelle Karas, Karolina Watts, Jeremy J. Rusjan, Pablo Houle, Sylvain Mizrahi, Romina Lower amygdala fatty acid amide hydrolase in violent offenders with antisocial personality disorder: an [(11)C]CURB positron emission tomography study |
title | Lower amygdala fatty acid amide hydrolase in violent offenders with antisocial personality disorder: an [(11)C]CURB positron emission tomography study |
title_full | Lower amygdala fatty acid amide hydrolase in violent offenders with antisocial personality disorder: an [(11)C]CURB positron emission tomography study |
title_fullStr | Lower amygdala fatty acid amide hydrolase in violent offenders with antisocial personality disorder: an [(11)C]CURB positron emission tomography study |
title_full_unstemmed | Lower amygdala fatty acid amide hydrolase in violent offenders with antisocial personality disorder: an [(11)C]CURB positron emission tomography study |
title_short | Lower amygdala fatty acid amide hydrolase in violent offenders with antisocial personality disorder: an [(11)C]CURB positron emission tomography study |
title_sort | lower amygdala fatty acid amide hydrolase in violent offenders with antisocial personality disorder: an [(11)c]curb positron emission tomography study |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7814116/ https://www.ncbi.nlm.nih.gov/pubmed/33462180 http://dx.doi.org/10.1038/s41398-020-01144-2 |
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