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1. Psychological trauma and the genetic overlap between posttraumatic stress disorder and major depressive disorder

Author

Mundy, Jessica, Hübel, Christopher, Gelernter, Joel, Levey, Daniel, Murray, Robin M, Skelton, Megan, Stein, Murray B, Maihofer, Adam X, Nievergelt, Caroline M, Baker, Dewlen G, Risborough, Victoria B, Calabrese, Joseph R, Galea, Sandro, Stein, Dan J, Koen, Nastassja, Dalvie, Shareefa, Aiello, Allison E, Roberts, Andrea L, Koenen, KC, Solovieff, Nadia, Kranzler, Henry R, Zhao, Hongyu, Farrer, Lindsay A, Johnson, Eric Otto, Rice, John P, Bierut, Laura J, Saccone, Nancy L, McFarlane, Alexander, Forbes, David, Silove, Derrick, O'Donnell, Meaghan, Bryant, Richard A, van Hooff, Miranda, Sponheim, Scott R, Disner, Seth G, Pietrzak, Robert H, Chen, Chia-Yen, Smoller, Jordan W, Ursano, Robert J, Kessler, Ronald C, Junglen, Angela G, Delahanty, Douglas L, Amstadter, Ananda B, Sheerin, Christina M, Ruggiero, Ken, McLaughlin, Katie A, Peverill, Matthew, Caldas-de-Almeida, JM, Austin, S Bryn, Gelaye, Bizu, Williams, Michelle A, Sanchez, Sixto E, Franz, Carol E, Panizzon, Matthew S, Lyons, Michael J, Kremen, William S, Andreassen, Ole A, Dale, Anders M, Rutten, Bart PF, Vinkers, Christiaan, Schijven, Dick, Geuze, Elbert, Vermetten, Eric, Luykx, Jurjen J, Boks, Marco P, Ashley-Koch, Allison E, Beckham, Jean C, Garrett, Melanie E, Hauser, Michael A, Dennis, Michelle F, Kimbrel, Nathan A, Qin, Xue-Jun, Karstoft, Karen-Inge, Andersen, Soren B, Borglum, Anders D, Hougaard, David Michael, Bybjerg-Grauholm, Jonas, Duncan, Laramie E, Bµkvad-Hansen, Marie, Nordentoft, Merete, Mors, Ole, Mortensen, PB, Werge, Thomas, Thompson, Wesley K, Wang, Yunpeng, Heath, Andrew C, Nelson, Elliot C, Martin, Nicholas G, Gordon, Scott D, Wolf, Erika J, Logue, Mark W, Miller, Mark W, McGlinchey, Regina E, Milberg, William, Erbes, Christopher R, Polusny, Melissa A, Arbisi, Paul A, and Peterson, Alan L

Subjects
Prevention, Clinical Research, Genetics, Serious Mental Illness, Depression, Post-Traumatic Stress Disorder (PTSD), Mental Health, Brain Disorders, Anxiety Disorders, Major Depressive Disorder, Human Genome, 2.3 Psychological, social and economic factors, Aetiology, Mental health, Good Health and Well Being, Posttraumatic stress disorder, major depressive disorder, psychological trauma, genetics, genetic correlations, polygenic risk scores, Million Veteran Program, Post Traumatic Stress Disorder Working Group of the Psychiatric Genomics Consortium, Neurosciences, Public Health and Health Services, Psychology, Psychiatry
Abstract

BackgroundPosttraumatic stress disorder (PTSD) and major depressive disorder (MDD) are commonly reported co-occurring mental health consequences of psychological trauma exposure. The disorders have high genetic overlap. Trauma is a complex phenotype but research suggests that trauma sensitivity has a heritable basis. We investigated whether sensitivity to trauma in those with MDD reflects a similar genetic component in those with PTSD.MethodsGenetic correlations between PTSD and MDD in individuals reporting trauma and MDD in individuals not reporting trauma were estimated, as well as with recurrent MDD and single-episode MDD, using genome-wide association study (GWAS) summary statistics. Genetic correlations were replicated using PTSD data from the Psychiatric Genomics Consortium and the Million Veteran Program. Polygenic risk scores were generated in UK Biobank participants who met the criteria for lifetime MDD (N = 29 471). We investigated whether genetic loading for PTSD was associated with reporting trauma in these individuals.ResultsGenetic loading for PTSD was significantly associated with reporting trauma in individuals with MDD [OR 1.04 (95% CI 1.01-1.07), Empirical-p = 0.02]. PTSD was significantly more genetically correlated with recurrent MDD than with MDD in individuals not reporting trauma (rg differences = ~0.2, p < 0.008). Participants who had experienced recurrent MDD reported significantly higher rates of trauma than participants who had experienced single-episode MDD (χ2 > 166, p < 0.001).ConclusionsOur findings point towards the existence of genetic variants associated with trauma sensitivity that might be shared between PTSD and MDD, although replication with better powered GWAS is needed. Our findings corroborate previous research highlighting trauma exposure as a key risk factor for recurrent MDD.

Published
2022

2. Enhancing Discovery of Genetic Variants for Posttraumatic Stress Disorder Through Integration of Quantitative Phenotypes and Trauma Exposure Information

Author

Maihofer, Adam X, Choi, Karmel W, Coleman, Jonathan RI, Daskalakis, Nikolaos P, Denckla, Christy A, Ketema, Elizabeth, Morey, Rajendra A, Polimanti, Renato, Ratanatharathorn, Andrew, Torres, Katy, Wingo, Aliza P, Zai, Clement C, Aiello, Allison E, Almli, Lynn M, Amstadter, Ananda B, Andersen, Soren B, Andreassen, Ole A, Arbisi, Paul A, Ashley-Koch, Allison E, Austin, S Bryn, Avdibegović, Esmina, Borglum, Anders D, Babić, Dragan, Bækvad-Hansen, Marie, Baker, Dewleen G, Beckham, Jean C, Bierut, Laura J, Bisson, Jonathan I, Boks, Marco P, Bolger, Elizabeth A, Bradley, Bekh, Brashear, Meghan, Breen, Gerome, Bryant, Richard A, Bustamante, Angela C, Bybjerg-Grauholm, Jonas, Calabrese, Joseph R, Caldas-de-Almeida, José M, Chen, Chia-Yen, Dale, Anders M, Dalvie, Shareefa, Deckert, Jürgen, Delahanty, Douglas L, Dennis, Michelle F, Disner, Seth G, Domschke, Katharina, Duncan, Laramie E, Džubur Kulenović, Alma, Erbes, Christopher R, Evans, Alexandra, Farrer, Lindsay A, Feeny, Norah C, Flory, Janine D, Forbes, David, Franz, Carol E, Galea, Sandro, Garrett, Melanie E, Gautam, Aarti, Gelaye, Bizu, Gelernter, Joel, Geuze, Elbert, Gillespie, Charles F, Goçi, Aferdita, Gordon, Scott D, Guffanti, Guia, Hammamieh, Rasha, Hauser, Michael A, Heath, Andrew C, Hemmings, Sian MJ, Hougaard, David Michael, Jakovljević, Miro, Jett, Marti, Johnson, Eric Otto, Jones, Ian, Jovanovic, Tanja, Qin, Xue-Jun, Karstoft, Karen-Inge, Kaufman, Milissa L, Kessler, Ronald C, Khan, Alaptagin, Kimbrel, Nathan A, King, Anthony P, Koen, Nastassja, Kranzler, Henry R, Kremen, William S, Lawford, Bruce R, Lebois, Lauren AM, Lewis, Catrin, Liberzon, Israel, Linnstaedt, Sarah D, Logue, Mark W, Lori, Adriana, Lugonja, Božo, Luykx, Jurjen J, Lyons, Michael J, Maples-Keller, Jessica L, Marmar, Charles, Martin, Nicholas G, Maurer, Douglas, and Mavissakalian, Matig R

Subjects
Biological Sciences, Genetics, Anxiety Disorders, Mental Health, Brain Disorders, Post-Traumatic Stress Disorder (PTSD), Prevention, Human Genome, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Phenotype, Polymorphism, Single Nucleotide, Stress Disorders, Post-Traumatic, GWAS, Heritability, PTSD, PheWAS, Trauma, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Biological sciences, Biomedical and clinical sciences, Psychology
Abstract

BackgroundPosttraumatic stress disorder (PTSD) is heritable and a potential consequence of exposure to traumatic stress. Evidence suggests that a quantitative approach to PTSD phenotype measurement and incorporation of lifetime trauma exposure (LTE) information could enhance the discovery power of PTSD genome-wide association studies (GWASs).MethodsA GWAS on PTSD symptoms was performed in 51 cohorts followed by a fixed-effects meta-analysis (N = 182,199 European ancestry participants). A GWAS of LTE burden was performed in the UK Biobank cohort (N = 132,988). Genetic correlations were evaluated with linkage disequilibrium score regression. Multivariate analysis was performed using Multi-Trait Analysis of GWAS. Functional mapping and annotation of leading loci was performed with FUMA. Replication was evaluated using the Million Veteran Program GWAS of PTSD total symptoms.ResultsGWASs of PTSD symptoms and LTE burden identified 5 and 6 independent genome-wide significant loci, respectively. There was a 72% genetic correlation between PTSD and LTE. PTSD and LTE showed largely similar patterns of genetic correlation with other traits, albeit with some distinctions. Adjusting PTSD for LTE reduced PTSD heritability by 31%. Multivariate analysis of PTSD and LTE increased the effective sample size of the PTSD GWAS by 20% and identified 4 additional loci. Four of these 9 PTSD loci were independently replicated in the Million Veteran Program.ConclusionsThrough using a quantitative trait measure of PTSD, we identified novel risk loci not previously identified using prior case-control analyses. PTSD and LTE have a high genetic overlap that can be leveraged to increase discovery power through multivariate methods.

Published
2022

4. The Relationship of Attention-Deficit/Hyperactivity Disorder With Posttraumatic Stress Disorder: A Two-Sample Mendelian Randomization and Population-Based Sibling Comparison Study

Author

Maihofer, Adam X., Choi, Karmel W., Coleman, Jonathan R.I., Daskalakis, Nikolaos P., Denckla, Christy A., Ketema, Elizabeth, Morey, Rajendra A., Polimanti, Renato, Ratanatharathorn, Andrew, Torres, Katy, Wingo, Aliza P., Zai, Clement C., Aiello, Allison E., Almli, Lynn M., Amstadter, Ananda B., Andersen, Soren B., Andreassen, Ole A., Arbisi, Paul A., Ashley-Koch, Allison E., Austin, S. Bryn, Avdibegovic, Esmina, Borglum, Anders D., Babic, Dragan, Bækvad-Hansen, Marie, Baker, Dewleen G., Beckham, Jean C., Bierut, Laura J., Bisson, Jonathan I., Boks, Marco P., Bolger, Elizabeth A., Bradley, Bekh, Brashear, Meghan, Breen, Gerome, Bryant, Richard A., Bustamante, Angela C., Bybjerg-Grauholm, Jonas, Calabrese, Joseph R., Caldas-de-Almeida, Jose Miguel, Chen, Chia-Yen, Dale, Anders M., Dalvie, Shareefa, Deckert, Jürgen, Delahanty, Douglas L., Dennis, Michelle F., Disner, Seth G., Domschke, Katharina, Duncan, Laramie E., Kulenovic, Alma Dzubur, Erbes, Christopher R., Evans, Alexandra, Farrer, Lindsay A., Feeny, Norah C., Flory, Janine D., Forbes, David, Franz, Carol E., Galea, Sandro, Garrett, Melanie E., Gautam, Aarti, Gelaye, Bizu, Gelernter, Joel, Geuze, Elbert, Gillespie, Charles F., Uka, Aferdita Goci, Gordon, Scott D., Guffanti, Guia, Hammamieh, Rasha, Hauser, Michael A., Heath, Andrew C., Hemmings, Sian M.J., Hougaard, David Michael, Jakovljevic, Miro, Jett, Marti, Johnson, Eric Otto, Jones, Ian, Jovanovic, Tanja, Qin, Xue-Jun, Karstoft, Karen-Inge, Kaufman, Milissa L., Kessler, Ronald C., Khan, Alaptagin, Kimbrel, Nathan A., King, Anthony P., Koen, Nastassja, Kranzler, Henry R., Kremen, William S., Lawford, Bruce R., Lebois, Lauren A.M., Lewis, Catrin, Liberzon, Israel, Linnstaedt, Sarah D., Logue, Mark W., Lori, Adriana, Lugonja, Bozo, Luykx, Jurjen J., Lyons, Michael J., Maples-Keller, Jessica L., Marmar, Charles, Martin, Nicholas G., Maurer, Douglas, Mavissakalian, Matig R., McFarlane, Alexander, McGlinchey, Regina E., McLaughlin, Katie A., McLean, Samuel A., Mehta, Divya, Mellor, Rebecca, Michopoulos, Vasiliki, Milberg, William, Miller, Mark W., Morris, Charles Phillip, Mors, Ole, Mortensen, Preben Bo, Nelson, Elliot C., Nordentoft, Merete, Norman, Sonya B., O’Donnell, Meaghan, Orcutt, Holly K., Panizzon, Matthew S., Peters, Edward S., Peterson, Alan L., Peverill, Matthew, Pietrzak, Robert H., Polusny, Melissa A., Rice, John P., Risbrough, Victoria B., Roberts, Andrea L., Rothbaum, Alex O., Rothbaum, Barbara O., Roy-Byrne, Peter, Ruggiero, Kenneth J., Rung, Ariane, Rutten, Bart P.F., Saccone, Nancy L., Sanchez, Sixto E., Schijven, Dick, Seedat, Soraya, Seligowski, Antonia V., Seng, Julia S., Sheerin, Christina M., Silove, Derrick, Smith, Alicia K., Smoller, Jordan W., Sponheim, Scott R., Stein, Dan J., Stevens, Jennifer S., Teicher, Martin H., Thompson, Wesley K., Trapido, Edward, Uddin, Monica, Ursano, Robert J., Luella van den Heuvel, Leigh, Van Hooff, Miranda, Vermetten, Eric, Vinkers, Christiaan, Voisey, Joanne, Wang, Yunpeng, Wang, Zhewu, Werge, Thomas, Williams, Michelle A., Williamson, Douglas E., Winternitz, Sherry, Wolf, Christiane, Wolf, Erika J., Yehuda, Rachel, Young, Keith A., Young, Ross McD., Zhao, Hongyu, Zoellner, Lori A., Haas, Magali, Lasseter, Heather, Provost, Allison C., Salem, Rany M., Sebat, Jonathan, Shaffer, Richard, Wu, Tianying, Ripke, Stephan, Daly, Mark J., Ressler, Kerry J., Koenen, Karestan C., Stein, Murray B., Nievergelt, Caroline M., Wendt, Frank R., Garcia-Argibay, Miguel, Cabrera-Mendoza, Brenda, Valdimarsdóttir, Unnur A., Nivard, Michel G., Larsson, Henrik, Mattheisen, Manuel, and Meier, Sandra M.

Published
2023
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5. International meta-analysis of PTSD genome-wide association studies identifies sex- and ancestry-specific genetic risk loci.

Author

Nievergelt, Caroline M, Maihofer, Adam X, Klengel, Torsten, Atkinson, Elizabeth G, Chen, Chia-Yen, Choi, Karmel W, Coleman, Jonathan RI, Dalvie, Shareefa, Duncan, Laramie E, Gelernter, Joel, Levey, Daniel F, Logue, Mark W, Polimanti, Renato, Provost, Allison C, Ratanatharathorn, Andrew, Stein, Murray B, Torres, Katy, Aiello, Allison E, Almli, Lynn M, Amstadter, Ananda B, Andersen, Søren B, Andreassen, Ole A, Arbisi, Paul A, Ashley-Koch, Allison E, Austin, S Bryn, Avdibegovic, Esmina, Babić, Dragan, Bækvad-Hansen, Marie, Baker, Dewleen G, Beckham, Jean C, Bierut, Laura J, Bisson, Jonathan I, Boks, Marco P, Bolger, Elizabeth A, Børglum, Anders D, Bradley, Bekh, Brashear, Megan, Breen, Gerome, Bryant, Richard A, Bustamante, Angela C, Bybjerg-Grauholm, Jonas, Calabrese, Joseph R, Caldas-de-Almeida, José M, Dale, Anders M, Daly, Mark J, Daskalakis, Nikolaos P, Deckert, Jürgen, Delahanty, Douglas L, Dennis, Michelle F, Disner, Seth G, Domschke, Katharina, Dzubur-Kulenovic, Alma, Erbes, Christopher R, Evans, Alexandra, Farrer, Lindsay A, Feeny, Norah C, Flory, Janine D, Forbes, David, Franz, Carol E, Galea, Sandro, Garrett, Melanie E, Gelaye, Bizu, Geuze, Elbert, Gillespie, Charles, Uka, Aferdita Goci, Gordon, Scott D, Guffanti, Guia, Hammamieh, Rasha, Harnal, Supriya, Hauser, Michael A, Heath, Andrew C, Hemmings, Sian MJ, Hougaard, David Michael, Jakovljevic, Miro, Jett, Marti, Johnson, Eric Otto, Jones, Ian, Jovanovic, Tanja, Qin, Xue-Jun, Junglen, Angela G, Karstoft, Karen-Inge, Kaufman, Milissa L, Kessler, Ronald C, Khan, Alaptagin, Kimbrel, Nathan A, King, Anthony P, Koen, Nastassja, Kranzler, Henry R, Kremen, William S, Lawford, Bruce R, Lebois, Lauren AM, Lewis, Catrin E, Linnstaedt, Sarah D, Lori, Adriana, Lugonja, Bozo, Luykx, Jurjen J, Lyons, Michael J, Maples-Keller, Jessica, Marmar, Charles, and Martin, Alicia R

Subjects
Humans, Genetic Predisposition to Disease, Ubiquitin-Protein Ligases, Stress Disorders, Post-Traumatic, Sex Factors, African Continental Ancestry Group, European Continental Ancestry Group, Veterans, Female, Male, Genome-Wide Association Study, Genetic Loci, Datasets as Topic, Human Genome, Mental Health, Biotechnology, Clinical Research, Post-Traumatic Stress Disorder (PTSD), Anxiety Disorders, Prevention, Genetics
Abstract

The risk of posttraumatic stress disorder (PTSD) following trauma is heritable, but robust common variants have yet to be identified. In a multi-ethnic cohort including over 30,000 PTSD cases and 170,000 controls we conduct a genome-wide association study of PTSD. We demonstrate SNP-based heritability estimates of 5-20%, varying by sex. Three genome-wide significant loci are identified, 2 in European and 1 in African-ancestry analyses. Analyses stratified by sex implicate 3 additional loci in men. Along with other novel genes and non-coding RNAs, a Parkinson's disease gene involved in dopamine regulation, PARK2, is associated with PTSD. Finally, we demonstrate that polygenic risk for PTSD is significantly predictive of re-experiencing symptoms in the Million Veteran Program dataset, although specific loci did not replicate. These results demonstrate the role of genetic variation in the biology of risk for PTSD and highlight the necessity of conducting sex-stratified analyses and expanding GWAS beyond European ancestry populations.

Published
2019

6. Multi-trait genome-wide association study of opioid addiction: OPRM1 and beyond

Author

Gaddis, Nathan, Mathur, Ravi, Marks, Jesse, Zhou, Linran, Quach, Bryan, Waldrop, Alex, Levran, Orna, Agrawal, Arpana, Randesi, Matthew, Adelson, Miriam, Jeffries, Paul W., Martin, Nicholas G., Degenhardt, Louisa, Montgomery, Grant W., Wetherill, Leah, Lai, Dongbing, Bucholz, Kathleen, Foroud, Tatiana, Porjesz, Bernice, Runarsdottir, Valgerdur, Tyrfingsson, Thorarinn, Einarsson, Gudmundur, Gudbjartsson, Daniel F., Webb, Bradley Todd, Crist, Richard C., Kranzler, Henry R., Sherva, Richard, Zhou, Hang, Hulse, Gary, Wildenauer, Dieter, Kelty, Erin, Attia, John, Holliday, Elizabeth G., McEvoy, Mark, Scott, Rodney J., Schwab, Sibylle G., Maher, Brion S., Gruza, Richard, Kreek, Mary Jeanne, Nelson, Elliot C., Thorgeirsson, Thorgeir, Stefansson, Kari, Berrettini, Wade H., Gelernter, Joel, Edenberg, Howard J., Bierut, Laura, Hancock, Dana B., and Johnson, Eric Otto

Published
2022
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7. Frequent Cocaine Use is Associated With Larger HIV Latent Reservoir Size.

Author

Aouizerat, Bradley E., Garcia, Josephine N., Domingues, Carlos V., Ke Xu, Quach, Bryan C., Page, Grier P., Konkle-Parker, Deborah, Bolivar, Hector H., Lahiri, Cecile D., Golub, Elizabeth T., Cohen, Mardge H., Kassaye, Seble G., DeHovitz, Jack, Kuniholm, Mark H., Archin, Nancie M., Tien, Phyllis C., Hancock, Dana B., and Johnson, Eric Otto

Published
2024
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8. Emerging Topics and Innovative Methodologies in Cannabis Research.

Author

Albright, Victoria A. and Johnson, Eric Otto

Subjects
*SUBSTANCE abuse & psychology, *CANNABIS (Genus), *SERIAL publications, *SOCIAL norms, *SOCIOECONOMIC factors
Abstract

Aims And Scope: Cannabis use is ascendant in our society, affecting the health of our citizens, our social norms and social structures, and our economies. This special issue brings together a diverse set of research manuscripts that push the borders of our understanding of burgeoning cannabis use and displays innovative methods developed to study these phenomena. [ABSTRACT FROM AUTHOR]

Published
2018
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9. Frequent Cocaine Use is Associated With Larger HIV Latent Reservoir Size.

Author

Aouizerat BE, Garcia JN, Domingues CV, Xu K, Quach BC, Page GP, Konkle-Parker D, Bolivar HH, Lahiri CD, Golub ET, Cohen MH, Kassaye SG, DeHovitz J, Kuniholm MH, Archin NM, Tien PC, Hancock DB, and Johnson EO

Subjects
Humans, Female, Adult, Middle Aged, Longitudinal Studies, HIV-1 genetics, United States epidemiology, DNA, Viral, Cocaine, HIV Infections drug therapy, CD4-Positive T-Lymphocytes, Viral Load, Virus Latency, Cocaine-Related Disorders epidemiology
Abstract

Background: Cocaine-one of the most frequently abused illicit drugs among persons living with HIV [people living with HIV (PLWH)]-slows the decline of viral production after antiretroviral therapy and is associated with higher HIV viral load, more rapid HIV progression, and increased mortality., Setting: We examined the impact of cocaine use on the CD4+ T-cell HIV latent reservoir (HLR) in virally suppressed PLWH participating in a national, longitudinal cohort study of the natural and treated history of HIV in the United States., Methods: CD4+ T-cell genomic DNA from 434 women of diverse ancestry (ie, 75% Black, 14% Hispanic, 12% White) who self-reported cocaine use (ie, 160 cocaine users, 59 prior users, 215 non-users) was analyzed using the Intact Proviral HIV DNA Assay, measuring intact provirus per 106 CD4+ T cells., Findings: HIV latent reservoir size differed by cocaine use (ie, median [interquartile range]: 72 [14-193] for never users, 165 [63-387] for prior users, 184 [28-502] for current users), which was statistically significantly larger in both prior (P = 0.023) and current (P = 0.001) cocaine users compared with never users., Conclusions: Cocaine use may contribute to a larger replication competent HLR in CD4+ T cells among virologically suppressed women living with HIV. Our findings are important because women are underrepresented in HIV reservoir studies and in studies of the impact of cocaine use on outcomes among PLWH., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Published
2024
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10. Identifying novel gene dysregulation associated with opioid overdose death: A meta-analysis of differential gene expression in human prefrontal cortex.

Author

Carter JK, Quach BC, Willis C, Minto MS, Hancock DB, Montalvo-Ortiz J, Corradin O, Logan RW, Walss-Bass C, Maher BS, and Johnson EO

Abstract

Only recently have human postmortem brain studies of differential gene expression (DGE) associated with opioid overdose death (OOD) been published; sample sizes from these studies have been modest (N = 40-153). To increase statistical power to identify OOD-associated genes, we leveraged human prefrontal cortex RNAseq data from four independent OOD studies and conducted a transcriptome-wide DGE meta-analysis (N = 285). Using a unified gene expression data processing and analysis framework across studies, we meta-analyzed 20 098 genes and found 335 significant differentially expressed genes (DEGs) by OOD status (false discovery rate < 0.05). Of these, 66 DEGs were among the list of 303 genes reported as OOD-associated in prior prefrontal cortex molecular studies, including genes/gene families (e.g., OPRK1, NPAS4 , DUSP, EGR ). The remaining 269 DEGs were not previously reported (e.g., NR4A2, SYT1, HCRTR2, BDNF ). There was little evidence of genetic drivers for the observed differences in gene expression between opioid addiction cases and controls. Enrichment analyses for the DEGs across molecular pathway and biological process databases highlight an interconnected set of genes and pathways from orexin and tyrosine kinase receptors through MEK/ERK/MAPK signaling to affect neuronal plasticity., Competing Interests: Conflict of Interest The authors declare no conflict of interest.

Published
2024
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11. Investigating the Relationship Between Smoking Behavior and Global Brain Volume.

Author

Chang Y, Thornton V, Chaloemtoem A, Anokhin AP, Bijsterbosch J, Bogdan R, Hancock DB, Johnson EO, and Bierut LJ

Abstract

Background: Previous studies have shown that brain volume is negatively associated with cigarette smoking, but there is an ongoing debate about whether smoking causes lowered brain volume or a lower brain volume is a risk factor for smoking. We address this debate through multiple methods that evaluate directionality: Bradford Hill's criteria, which are commonly used to understand a causal relationship in epidemiological studies, and mediation analysis., Methods: In 32,094 participants of European descent from the UK Biobank dataset, we examined the relationship between a history of daily smoking and brain volumes, as well as an association of genetic risk score to ever smoking with brain volume., Results: A history of daily smoking was strongly associated with decreased brain volume, and a history of heavier smoking was associated with a greater decrease in brain volume. The strongest association was between total gray matter volume and a history of daily smoking (effect size = -2964 mm 3 , p  = 2.04 × 10 -16 ), and there was a dose-response relationship with more pack years smoked associated with a greater decrease in brain volume. A polygenic risk score for smoking initiation was strongly associated with a history of daily smoking (effect size = 0.05, p  = 4.20 × 10 -84 ), but only modestly associated with total gray matter volume (effect size = -424 mm 3 , p  = .01). Mediation analysis indicated that a history of daily smoking mediated the relationship between the smoking initiation polygenic risk score and total gray matter volume., Conclusions: A history of daily smoking is strongly associated with a decreased total brain volume., (© 2023 Published by Elsevier Inc on behalf of Society of Biological Psychiatry.)

Published
2023
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