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Post-Traumatic Stress Disorders: HELP
Articles by Erika J. Wolf
Based on 67 articles published since 2010
(Why 67 articles?)
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Between 2010 and 2020, E. J. Wolf wrote the following 67 articles about Stress Disorders, Post-Traumatic.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3
1 Review DNA methylation correlates of PTSD: Recent findings and technical challenges. 2019

Morrison, Filomene G / Miller, Mark W / Logue, Mark W / Assef, Michele / Wolf, Erika J. ·National Center for PTSD, VA Boston Healthcare System, USA; Department of Psychiatry, Boston University School of Medicine, USA. Electronic address: filomene@bu.edu. · National Center for PTSD, VA Boston Healthcare System, USA; Department of Psychiatry, Boston University School of Medicine, USA. · National Center for PTSD, VA Boston Healthcare System, USA; Department of Psychiatry, Boston University School of Medicine, USA; Biomedical Genetics, Boston University School of Medicine, USA; Department of Biostatistics, Boston University School of Public Health, USA. · Boston University, College of Health & Rehabilitation Sciences: Sargent College, USA. ·Prog Neuropsychopharmacol Biol Psychiatry · Pubmed #30503303.

ABSTRACT: There is increasing evidence that epigenetic factors play a critical role in posttraumatic stress disorder (PTSD), by mediating the impact of environmental exposures to trauma on the regulation of gene expression. DNA methylation is one epigenetic process that has been highly studied in PTSD. This review will begin by providing an overview of DNA methylation (DNAm) methods, and will then highlight two major biological systems that have been identified in the epigenetic regulation in PTSD: (a) the immune system and (b) the stress response system. In addition to candidate gene approaches, we will review novel strategies to study epigenome-wide PTSD-related effects, including epigenome-wide algorithms that distill information from many loci into a single summary score (e.g., measures of "epigenetic age" which have been associated with PTSD). This review will also cover recent epigenome wide association studies (EWAS) of PTSD, and biological pathway models used to identify gene sets enriched in PTSD. Finally, we address technical and methodological advances and challenges to the field, and highlight exciting directions for future research.

2 Review Oxidative Stress, Inflammation, and Neuroprogression in Chronic PTSD. 2018

Miller, Mark W / Lin, Alex P / Wolf, Erika J / Miller, Danielle R. ·From the Department of Psychiatry, Boston University School of Medicine (Drs. M. W. Miller, Wolf, and D. R. Miller) · National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, MA (Drs. M. W. Miller, Wolf, and D. R. Miller) · Harvard Medical School and Department of Radiology, Brigham & Women's Hospital, Boston, MA (Dr. Lin). ·Harv Rev Psychiatry · Pubmed #29016379.

ABSTRACT: Posttraumatic stress disorder is a serious and often disabling syndrome that develops in response to a traumatic event. Many individuals who initially develop the disorder go on to experience a chronic form of the condition that in some cases can last for many years. Among these patients, psychiatric and medical comorbidities are common, including early onset of age-related conditions such as chronic pain, cardiometabolic disease, neurocognitive disorders, and dementia. The hallmark symptoms of posttraumatic stress-recurrent sensory-memory reexperiencing of the trauma(s)-are associated with concomitant activations of threat- and stress-related neurobiological pathways that occur against a tonic backdrop of sleep disturbance and heightened physiological arousal. Emerging evidence suggests that the molecular consequences of this stress-perpetuating syndrome include elevated systemic levels of oxidative stress and inflammation. In this article we review evidence for the involvement of oxidative stress and inflammation in chronic PTSD and the neurobiological consequences of these processes, including accelerated cellular aging and neuroprogression. Our aim is to update and expand upon previous reviews of this rapidly developing literature and to discuss magnetic resonance spectroscopy as an imaging technology uniquely suited to measuring oxidative stress and inflammatory markers in vivo. Finally, we highlight future directions for research and avenues for the development of novel therapeutics targeting oxidative stress and inflammation in patients with PTSD.

3 Review Traumatic Stress and Accelerated Cellular Aging: From Epigenetics to Cardiometabolic Disease. 2017

Wolf, Erika J / Morrison, Filomene G. ·National Center for PTSD, VA Boston Healthcare System, (116B-2), 150 South Huntington Ave, Boston, MA, 02130, USA. erika.wolf@va.gov. · Department of Psychiatry, Boston University School of Medicine, Boston, MA, USA. erika.wolf@va.gov. · McLean Hospital, Harvard Medical School, Belmont, MA, USA. ·Curr Psychiatry Rep · Pubmed #28852965.

ABSTRACT: PURPOSE OF REVIEW: The aim of this paper is to review the recent literature on traumatic stress-related accelerated aging, including a focus on cellular mechanisms and biomarkers of cellular aging and on the clinical manifestations of accelerated biological aging. RECENT FINDINGS: Multiple lines of research converge to suggest that PTSD is associated with accelerated aging in the epigenome, and the immune and inflammation systems, and this may be reflected in premature onset of cardiometabolic and cardiovascular disease. The current state of research paves the way for future work focused on identifying the peripheral and central biological mechanisms linking traumatic stress to accelerated biological aging and medical morbidity, with an emphasis on processes involved in inflammation, immune functioning, oxidative stress, autonomic arousal, and stress response. Ultimately, such work could help reduce the pace of biological aging and improve health and wellness.

4 Review A critical evaluation of the complex PTSD literature: implications for DSM-5. 2012

Resick, Patricia A / Bovin, Michelle J / Calloway, Amber L / Dick, Alexandra M / King, Matthew W / Mitchell, Karen S / Suvak, Michael K / Wells, Stephanie Y / Stirman, Shannon Wiltsey / Wolf, Erika J. ·National Center for Posttraumatic Stress Disorder, VA Boston Healthcare System, Boston, MA 02130, USA. Patricia.Resick@va.gov ·J Trauma Stress · Pubmed #22729974.

ABSTRACT: Complex posttraumatic stress disorder (CPTSD) has been proposed as a diagnosis for capturing the diverse clusters of symptoms observed in survivors of prolonged trauma that are outside the current definition of PTSD. Introducing a new diagnosis requires a high standard of evidence, including a clear definition of the disorder, reliable and valid assessment measures, support for convergent and discriminant validity, and incremental validity with respect to implications for treatment planning and outcome. In this article, the extant literature on CPTSD is reviewed within the framework of construct validity to evaluate the proposed diagnosis on these criteria. Although the efforts in support of CPTSD have brought much needed attention to limitations in the trauma literature, we conclude that available evidence does not support a new diagnostic category at this time. Some directions for future research are suggested.

5 Article International meta-analysis of PTSD genome-wide association studies identifies sex- and ancestry-specific genetic risk loci. 2019

Nievergelt, Caroline M / Maihofer, Adam X / Klengel, Torsten / Atkinson, Elizabeth G / Chen, Chia-Yen / Choi, Karmel W / Coleman, Jonathan R I / 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 M J / 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 A M / Lewis, Catrin E / Linnstaedt, Sarah D / Lori, Adriana / Lugonja, Bozo / Luykx, Jurjen J / Lyons, Michael J / Maples-Keller, Jessica / Marmar, Charles / Martin, Alicia R / Martin, Nicholas G / Maurer, Douglas / Mavissakalian, Matig R / McFarlane, Alexander / McGlinchey, Regina E / McLaughlin, Katie A / McLean, Samuel A / McLeay, Sarah / Mehta, Divya / Milberg, William P / Miller, Mark W / Morey, Rajendra A / Morris, Charles Phillip / Mors, Ole / Mortensen, Preben B / Neale, Benjamin M / 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 / Ripke, Stephan / Risbrough, Victoria B / Roberts, Andrea L / Rothbaum, Alex O / Rothbaum, Barbara O / Roy-Byrne, Peter / Ruggiero, Ken / 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 / Sumner, Jennifer A / Teicher, Martin H / Thompson, Wesley K / Trapido, Edward / Uddin, Monica / Ursano, Robert J / van den Heuvel, Leigh Luella / Van Hooff, Miranda / Vermetten, Eric / Vinkers, Christiaan H / Voisey, Joanne / Wang, Yunpeng / Wang, Zhewu / Werge, Thomas / Williams, Michelle A / Williamson, Douglas E / Winternitz, Sherry / Wolf, Christiane / Wolf, Erika J / Wolff, Jonathan D / Yehuda, Rachel / Young, Ross McD / Young, Keith A / Zhao, Hongyu / Zoellner, Lori A / Liberzon, Israel / Ressler, Kerry J / Haas, Magali / Koenen, Karestan C. ·University of California San Diego, Department of Psychiatry, La Jolla, CA, USA. cnievergelt@ucsd.edu. · Veterans Affairs San Diego Healthcare System, Center of Excellence for Stress and Mental Health, San Diego, CA, USA. cnievergelt@ucsd.edu. · Veterans Affairs San Diego Healthcare System, Research Service, San Diego, CA, USA. cnievergelt@ucsd.edu. · University of California San Diego, Department of Psychiatry, La Jolla, CA, USA. · Veterans Affairs San Diego Healthcare System, Center of Excellence for Stress and Mental Health, San Diego, CA, USA. · Veterans Affairs San Diego Healthcare System, Research Service, San Diego, CA, USA. · Harvard Medical School, Department of Psychiatry, Boston, MA, USA. · McLean Hospital, Belmont, MA, USA. · University Medical Center Goettingen, Department of Psychiatry, Göttingen, DE, Germany. · Broad Institute of MIT and Harvard, Stanley Center for Psychiatric Research, Cambridge, MA, USA. · Massachusetts General Hospital, Analytic and Translational Genetics Unit, Boston, MA, USA. · Massachusetts General Hospital, Psychiatric and Neurodevelopmental Genetics Unit (PNGU), Boston, MA, USA. · Massachusetts General Hospital, Department of Psychiatry, Boston, MA, USA. · Harvard T.H. Chan School of Public Health, Department of Epidemiology, Boston, MA, USA. · King's College London, Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, London, GB, USA. · King's College London, NIHR BRC at the Maudsley, London, GB, USA. · University of Cape Town, SA MRC Unit on Risk & Resilience in Mental Disorders, Department of Psychiatry, Cape Town, Western Cape, ZA, USA. · Stanford University, Department of Psychiatry and Behavioral Sciences, Stanford, CA, USA. · US Department of Veterans Affairs, Department of Psychiatry, West Haven, CT, USA. · Yale University School of Medicine, Department of Genetics and Neuroscience, New Haven, CT, USA. · VA Connecticut Healthcare Center, West Haven, CT, USA. · Yale University School of Medicine, Department of Psychiatry, New Haven, CT, USA. · VA Boston Healthcare System, National Center for PTSD, Boston, MA, USA. · Cohen Veterans Bioscience, Cambridge, MA, USA. · Veterans Affairs San Diego Healthcare System, Million Veteran Program, San Diego, CA, USA. · Veterans Affairs San Diego Healthcare System, Psychiatry Service, San Diego, CA, USA. · Gillings School of Global Public Health, Department of Epidemiology, Chapel Hill, NC, USA. · Emory University, Department of Psychiatry and Behavioral Sciences, Atlanta, GA, USA. · Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Richmond, VA, USA. · The Danish Veteran Centre, Research and Knowledge Centre, Ringsted, Sjaelland, Denmark. · University of Oslo, Institute of Clinical Medicine, Oslo, NO, Norway. · Minneapolis VA Health Care System, Mental Health Service Line, Minneapolis, MN, USA. · Duke University, Duke Molecular Physiology Institute, Durham, NC, USA. · Boston Children's Hospital, Division of Adolescent and Young Adult Medicine, Boston, MA, USA. · Brigham and Women's Hospital, Channing Division of Network Medicine, Boston, MA, USA. · Harvard School of Public Health, Department of Social and Behavioral Sciences, Boston, MA, USA. · University Clinical Center of Tuzla, Department of Psychiatry, Tuzla, BA, Bosnia and Herzegovina. · University Clinical Center of Mostar, Department of Psychiatry, Mostar, BA, Bosnia and Herzegovina. · Statens Serum Institut, Department for Congenital Disorders, Copenhagen, DK, Denmark. · The Lundbeck Foundation Initiative for Integrative Psychiatric Research, iPSYCH, DK, Denmark. · Durham VA Medical Center, Research, Durham, NC, USA. · Duke University, Department of Psychiatry and Behavioral Sciences, Durham, NC, USA. · VA Mid-Atlantic Mental Illness Research, Education, and Clinical Center (MIRECC), Genetics Research Laboratory, Durham, NC, USA. · Washington University in Saint Louis School of Medicine, Department of Psychiatry, Saint Louis, MO, USA. · Cardiff University, National Centre for Mental Health, MRC Centre for Psychiatric Genetics and Genomics, Cardiff, UK. · UMC Utrecht Brain Center Rudolf Magnus, Department of Translational Neuroscience, Utrecht, Utrecht, NL, Netherlands. · Aarhus University, Centre for Integrative Sequencing, iSEQ, Aarhus, DK, Denmark. · Aarhus University, Department of Biomedicine - Human Genetics, Aarhus, DK, Denmark. · Atlanta VA Health Care System, Mental Health Service Line, Decatur, GA, USA. · Louisiana State University Health Sciences Center, School of Public Health and Department of Epidemiology, New Orleans, LA, USA. · University of New South Wales, Department of Psychology, Sydney, NSW, Australia. · University of Michigan Medical School, Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Ann Arbor, MI, USA. · University Hospitals, Department of Psychiatry, Cleveland, OH, USA. · CEDOC -Chronic Diseases Research Centre, Lisbon Institute of Global Mental Health, Lisbon, PT, Portugal. · University of California San Diego, Department of Radiology, Department of Neurosciences, La Jolla, CA, USA. · Icahn School of Medicine at Mount Sinai, Department of Psychiatry, New York, NY, USA. · University Hospital of Würzburg, Center of Mental Health, Psychiatry, Psychosomatics and Psychotherapy, Würzburg, DE, Germany. · Kent State University, Department of Psychological Sciences, Kent, OH, USA. · Kent State University, Research and Sponsored Programs, Kent, OH, USA. · Minneapolis VA Health Care System, Research Service Line, Minneapolis, MN, USA. · Medical Center-University of Freiburg, Faculty of Medicine, Department of Psychiatry and Psychotherapy, Freiburg, DE, Germany. · University of Freiburg, Faculty of Medicine, Centre for Basics in Neuromodulation, Freiburg, DE, Germany. · University Clinical Center of Sarajevo, Department of Psychiatry, Sarajevo, BA, Bosnia and Herzegovina. · University of Minnesota, Department of Psychiatry, Minneapolis, MN, USA. · Minneapolis VA Health Care System, Center for Care Delivery and Outcomes Research (CCDOR), Minneapolis, MN, USA. · Cardiff University, National Centre for Mental Health, MRC Centre for Psychiatric Genetics and Genomics, Cardiff, South Glamorgan, GB, USA. · Boston University School of Medicine, Department of Medicine, Boston, MA, USA. · Case Western Reserve University, Department of Psychological Sciences, Cleveland, OH, USA. · University of Melbourne, Department of Psychiatry, Melbourne, VIC, AU, USA. · Boston University, Department of Psychological and Brain Sciences, Boston, MA, USA. · Netherlands Ministry of Defence, Brain Research and Innovation Centre, Utrecht, Utrecht, NL, Netherlands. · UMC Utrecht Brain Center Rudolf Magnus, Department of Psychiatry, Utrecht, Utrecht, NL, Netherlands. · University Clinical Centre of Kosovo, Department of Psychiatry, Prishtina, Kosovo, XK, USA. · QIMR Berghofer Medical Research Institute, Department of Genetics and Computational Biology, Brisbane, Queensland, Australia. · US Army Medical Research and Materiel Command, USACEHR, Fort Detrick, MD, USA. · Washington University in Saint Louis School of Medicine, Department of Genetics, Saint Louis, MO, USA. · Stellenbosch University Faculty of Medicine and Health Sciences, Department of Psychiatry, Cape Town, Western Cape, ZA, South Africa. · University Hospital Center of Zagreb, Department of Psychiatry, Zagreb, HR, USA. · RTI International, Behavioral Health and Criminal Justice Division, Research Triangle Park, NC, USA. · University of Copenhagen, Department of Psychology, Copenhagen, DK, Denmark. · Harvard Medical School, Department of Health Care Policy, Boston, MA, USA. · University of Michigan Medical School, Department of Psychiatry, Ann Arbor, MI, USA. · University of Pennsylvania Perelman School of Medicine, Department of Psychiatry, Philadelphia, PA, USA. · Mental Illness Research, Education and Clinical Center, Crescenz VAMC, Philadelphia, PA, USA. · Queensland University of Technology, Institute of Health and Biomedical Innovation, Kelvin Grove, QLD, AU, Australia. · Queensland University of Technology, School of Biomedical Sciences, Kelvin Grove, QLD, AU, Australia. · UNC Institute for Trauma Recovery, Department of Anesthesiology, Chapel Hill, NC, USA. · Emory University, Department of Gynecology and Obstetrics, Atlanta, GA, USA. · Boston University, Dean's Office, Boston, MA, USA. · New York University School of Medicine, Department of Psychiatry, New York, NY, USA. · United States Army, Command, Fort Sill, OK, USA. · University of Adelaide, Department of Psychiatry, Adelaide, South Australia, AU, Australia. · VA Boston Health Care System, GRECC/TRACTS, Boston, MA, USA. · Harvard University, Department of Psychology, Boston, MA, USA. · UNC Institute for Trauma Recovery, Department of Emergency Medicine, Chapel Hill, NC, USA. · Gallipoli Medical Research Institute, PTSD Initiative, Greenslopes, Queensland, AU, Australia. · Queensland University of Technology, School of Psychology and Counseling, Faculty of Health, Kelvin Grove, QLD, AU, Australia. · Aarhus University Hospital, Psychosis Research Unit, Risskov, DK, Denmark. · Aarhus University, Centre for Integrated Register-based Research, Aarhus, DK, Denmark. · Aarhus University, National Centre for Register-Based Research, Aarhus, DK, Denmark. · University of Copenhagen, Mental Health Services in the Capital Region of Denmark, Mental Health Center Copenhagen, Copenhagen, DK, Denmark. · Veterans Affairs San Diego Healthcare System, Department of Research and Psychiatry, San Diego, CA, USA. · National Center for Post Traumatic Stress Disorder, Executive Division, White River Junction, San Diego, VT, USA. · Northern Illinois University, Department of Psychology, DeKalb, IL, USA. · University of Texas Health Science Center at San Antonio, Department of Psychiatry, San Antonio, TX, USA. · University of Washington, Department of Psychology, Seattle, WA, USA. · U.S. Department of Veterans Affairs National Center for Posttraumatic Stress Disorder, West Haven, CT, USA. · Minneapolis VA Health Care System, Department of Mental Health, Minneapolis, MN, USA. · Minneapolis VA Health Care System, Department of Psychology, Minneapolis, MN, USA. · Charité - Universitätsmedizin, Department of Psychiatry and Psychotherapy, Berlin, GE, Germany. · Harvard T.H. Chan School of Public Health, Department of Environmental Health, Boston, MA, USA. · Medical University of South Carolina, Department of Nursing and Department of Psychiatry, Charleston, SC, USA. · Maastricht Universitair Medisch Centrum, School for Mental Health and Neuroscience, Department of Psychiatry and Neuropsychology, Maastricht, Limburg, NL, Netherlands. · Universidad Peruana de Ciencias Aplicadas Facultad de Ciencias de la Salud, Department of Medicine, Lima, Lima, PE, USA. · University of Michigan, School of Nursing, Ann Arbor, MI, USA. · University of New South Wales, Department of Psychiatry, Sydney, NSW, AU, USA. · Columbia University Medical Center, Department of Medicine, New York, NY, USA. · Mental Health Centre Sct. Hans, Institute of Biological Psychiatry, Roskilde, DK, Denmark. · Oslo University Hospital, KG Jebsen Centre for Psychosis Research, Norway Division of Mental Health and Addiction, Oslo, NO, USA. · University of South Florida College of Public Health, Genomics Program, Tampa, FL, USA. · Uniformed Services University, Department of Psychiatry, Bethesda, Maryland, USA. · Arq, Psychotrauma Reseach Expert Group, Diemen, NH, Netherlands. · Leiden University Medical Center, Department of Psychiatry, Leiden, ZH, NL, Netherlands. · Netherlands Defense Department, Research Center, Utrecht, UT, Netherlands. · Amsterdam UMC (location VUmc), Department of Anatomy and Neurosciences, Amsterdam, Holland, NL, Netherlands. · Amsterdam UMC (location VUmc), Department of Psychiatry, Amsterdam, Holland, NL, Netherlands. · Ralph H Johnson VA Medical Center, Department of Mental Health, Charleston, SC, USA. · Medical University of South Carolina, Department of Psychiatry and Behavioral Sciences, Charleston, SC, USA. · University of Copenhagen, Department of Clinical Medicine, Copenhagen, Denmark. · James J Peters VA Medical Center, Department of Mental Health, Bronx, NY, USA. · Baylor Scott and White Central Texas, Department of Psychiatry, Temple, TX, USA. · CTVHCS, COE for Research on Returning War Veterans, Waco, TX, USA. · Yale University, Department of Biostatistics, New Haven, CT, USA. · University of Washington, Department of Psychiatry and Behavioral Sciences, Seattle, WA, USA. · Harvard School of Public Health, Department of Epidemiology, Boston, MA, USA. ·Nat Commun · Pubmed #31594949.

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.

6 Article The PPM1F gene moderates the association between PTSD and cortical thickness. 2019

Sullivan, Danielle R / Morrison, Filomene G / Wolf, Erika J / Logue, Mark W / Fortier, Catherine B / Salat, David H / Fonda, Jennifer R / Stone, Annjanette / Schichman, Steven / Milberg, William / McGlinchey, Regina / Miller, Mark W. ·National Center for PTSD, VA Boston Healthcare System, Boston, MA, United States; Department of Psychiatry, Boston University School of Medicine, Boston, MA, United States. Electronic address: drsulliv@bu.edu. · National Center for PTSD, VA Boston Healthcare System, Boston, MA, United States; Department of Psychiatry, Boston University School of Medicine, Boston, MA, United States. · National Center for PTSD, VA Boston Healthcare System, Boston, MA, United States; Biomedical Genetics, Boston University School of Medicine, Boston, MA, United States; Department of Biostatistics, Boston University School of Public Health, Boston, MA, United States. · Translational Research Center for TBI and Stress Disorders (TRACTS) and Geriatric Research, Educational and Clinical Center (GRECC), VA Boston Healthcare System, Boston, MA, United States; Department of Psychiatry, Harvard Medical School, Boston, MA, United States. · Translational Research Center for TBI and Stress Disorders (TRACTS) and Geriatric Research, Educational and Clinical Center (GRECC), VA Boston Healthcare System, Boston, MA, United States; Neuroimaging Research for Veterans Center, VA Boston Healthcare System, Boston, MA, United States; Anthinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, United States. · Translational Research Center for TBI and Stress Disorders (TRACTS) and Geriatric Research, Educational and Clinical Center (GRECC), VA Boston Healthcare System, Boston, MA, United States; Department of Psychiatry, Boston University School of Medicine, Boston, MA, United States; Department of Psychiatry, Harvard Medical School, Boston, MA, United States. · Pharmacogenomics Analysis Laboratory, Research Service, Central Arkansas Veterans Healthcare System, Little Rock, AK, United States. ·J Affect Disord · Pubmed #31446381.

ABSTRACT: BACKGROUND: Evidence suggests that single nucleotide polymorphisms (SNPs) in genes involved in serotonergic signaling and stress response pathways moderate associations between PTSD and cortical thickness. This study examined a genetic regulator of these pathways, the PPM1F gene, which has also been implicated in mechanisms of stress responding and is differentially expressed in individuals with comorbid PTSD and depression compared to controls. METHODS: Drawing from a sample of 240 white non-Hispanic trauma-exposed veterans, we tested 18 SNPs spanning the PPM1F gene for association with PTSD and cortical thickness. RESULTS: Analyses revealed six PPM1F SNPs that moderated associations between PTSD symptom severity and cortical thickness of bilateral superior frontal and orbitofrontal regions as well as the right pars triangularis (all corrected p's < 0.05) such that greater PTSD severity was related to reduced cortical thickness as a function of genotype. A whole-cortex vertex-wise analysis using the most associated SNP (rs9610608) revealed this effect to be localized to a cluster in the right superior frontal gyrus (cluster-corrected p < 0.02). LIMITATIONS: Limitations of this study include the small sample size and that the sample was all-white, non-Hispanic predominately male veterans. CONCLUSIONS: These results extend prior work linking PPM1F to PTSD and suggest that variants in this gene may have bearing on the neural integrity of the prefrontal cortex (PFC).

7 Article Psychometric Properties of the Dissociative Subtype of PTSD Scale: Replication and Extension in a Clinical Sample of Trauma-Exposed Veterans. 2019

Guetta, Rachel E / Wilcox, Elizabeth S / Stoop, Tawni B / Maniates, Hannah / Ryabchenko, Karen A / Miller, Mark W / Wolf, Erika J. ·National Center for PTSD at VA Boston Healthcare System. · National Center for PTSD at VA Boston Healthcare System; Boston University School of Medicine. · National Center for PTSD at VA Boston Healthcare System; Boston University School of Medicine. Electronic address: Erika.Wolf@va.gov. ·Behav Ther · Pubmed #31422850.

ABSTRACT: The addition of the dissociative subtype of posttraumatic stress disorder (PTSD) to the DSM-5 has spurred investigation of its genetic, neurobiological, and treatment response correlates. In order to reliably assess the subtype, we developed the Dissociative Subtype of PTSD Scale (DSPS; Wolf et al., 2017), a 15-item index of dissociative features. Our initial investigation of the dichotomous DSPS lifetime items in a veteran epidemiological sample demonstrated its ability to identify the subtype, supported a three-factor measurement structure, distinguished the three subscales from the normal-range trait of absorption, and demonstrated the greater contribution of derealization and depersonalization symptoms relative to other dissociative symptomatology. In this study, we replicated and extended these findings by administering self-report and interview versions of the DSPS, and assessing personality and PTSD in a sample of 209 trauma-exposed veterans (83.73% male, 57.9% with probable current PTSD). Results replicated the three-factor structure using confirmatory factor analysis of current symptom severity interview items, and the identification of the dissociative subtype (via latent profile analysis). Associations with personality supported the discriminant validity of the DSPS and suggested the subtype was marked by tendencies towards odd and unusual cognitive experiences and low positive affect. Receiver operating characteristic curves identified diagnostic cut-points on the DSPS to inform subtype classification, which differed across the interview and self-report versions. Overall, the DSPS performed well in psychometric analyses, and results support the utility of the measure in identifying this important component of posttraumatic psychopathology.

8 Article Reduced interleukin 1A gene expression in the dorsolateral prefrontal cortex of individuals with PTSD and depression. 2019

Morrison, Filomene G / Miller, Mark W / Wolf, Erika J / Logue, Mark W / Maniates, Hannah / Kwasnik, David / Cherry, Jonathan D / Svirsky, Sarah / Restaino, Anthony / Hildebrandt, Audrey / Aytan, Nurgül / Stein, Thor D / Alvarez, Victor E / McKee, Ann C / Anonymous7481115 / Huber, Bertrand R. ·National Center for PTSD at VA Boston Healthcare System, United States; Department of Psychiatry, Boston University School of Medicine, United States. · National Center for PTSD at VA Boston Healthcare System, United States; Department of Psychiatry, Boston University School of Medicine, United States; Biomedical Genetics, Boston University School of Medicine, United States; Department of Biostatistics, Boston University School of Public Health, United States. · National Center for PTSD at VA Boston Healthcare System, United States. · Department of Psychiatry, Boston University School of Medicine, United States. · Department of Neurology, Boston University School of Medicine, United States. · Pathology and Laboratory Medicine, VA Boston Healthcare System, United States; Department of Neurology, Boston University School of Medicine, United States. · National Center for PTSD at VA Boston Healthcare System, United States; Pathology and Laboratory Medicine, VA Boston Healthcare System, United States. · Pathology and Laboratory Medicine, VA Boston Healthcare System, United States; Department of Neurology, Boston University School of Medicine, United States; Department of Pathology, Boston University School of Medicine, United States. · National Center for PTSD at VA Boston Healthcare System, United States; Pathology and Laboratory Medicine, VA Boston Healthcare System, United States; Department of Neurology, Boston University School of Medicine, United States. · National Center for PTSD at VA Boston Healthcare System, United States; Pathology and Laboratory Medicine, VA Boston Healthcare System, United States; Department of Neurology, Boston University School of Medicine, United States. Electronic address: Bertrand.huber@va.gov. ·Neurosci Lett · Pubmed #30366016.

ABSTRACT: The inflammatory system has been implicated in the pathophysiology of a variety of psychiatric conditions. Individuals with PTSD, depression, and other fear- and anxiety-related disorders exhibit alterations in peripheral circulating inflammatory markers, suggesting dysregulation of the inflammatory system. The relationship between inflammation and PTSD has been investigated almost exclusively in the periphery, and has not been extensively explored in human postmortem brain tissue. Interleukins (ILs) represent a subtype of cytokines and are key signaling proteins in the immune and inflammatory systems. Based on prior research implicating IL signaling in PTSD and depression, we performed a preliminary investigation of IL gene expression in a region of the cortex involved in emotion regulation and PTSD, the dorsolateral prefrontal cortex (dlPFC), using tissue from the newly established VA National PTSD Brain Bank. Gene expression analyses were conducted on post-mortem tissue from the dlPFC from 50 donors: 13 controls, 12 PTSD cases, and 25 depressed cases. RNA was extracted from frozen dlPFC tissue, reverse transcribed to cDNA, and quantitative polymerase chain reaction (qPCR) was performed to assess gene expression of IL1A, IL1B, IL6, IL8, IL10, IL13, and IL15. We found a multiple-testing corrected significant decrease in IL1A expression in the dlPFC for PTSD and depression cases compared to controls (p < 0.005) with age at death, sex, race and RNA integrity number (RIN) included as covariates. To our knowledge this finding is the first demonstration of altered IL expression in brain tissue from deceased individuals with histories of PTSD and/or depression.

9 Article Posttraumatic psychopathology and the pace of the epigenetic clock: a longitudinal investigation. 2019

Wolf, Erika J / Logue, Mark W / Morrison, Filomene G / Wilcox, Elizabeth S / Stone, Annjanette / Schichman, Steven A / McGlinchey, Regina E / Milberg, William P / Miller, Mark W. ·National Center for PTSD at VA Boston Healthcare System,Boston,MA 02130,USA. · Pharmacogenomics Analysis Laboratory,Research Service, Central Arkansas Veterans Healthcare System,Little Rock,AR,USA. · Geriatric Research Educational and Clinical Center and Translational Research Center for TBI and Stress Disorders, VA Boston Healthcare System,Boston,MA,USA. ·Psychol Med · Pubmed #29897034.

ABSTRACT: BACKGROUND: Posttraumatic stress disorder (PTSD) and stress/trauma exposure are cross-sectionally associated with advanced DNA methylation age relative to chronological age. However, longitudinal inquiry and examination of associations between advanced DNA methylation age and a broader range of psychiatric disorders is lacking. The aim of this study was to examine if PTSD, depression, generalized anxiety, and alcohol-use disorders predicted acceleration of DNA methylation age over time (i.e. an increasing pace, or rate of advancement, of the epigenetic clock). METHODS: Genome-wide DNA methylation and a comprehensive set of psychiatric symptoms and diagnoses were assessed in 179 Iraq/Afghanistan war veterans who completed two assessments over the course of approximately 2 years. Two DNA methylation age indices (Horvath and Hannum), each a weighted index of an array of genome-wide DNA methylation probes, were quantified. The pace of the epigenetic clock was operationalized as change in DNA methylation age as a function of time between assessments. RESULTS: Analyses revealed that alcohol-use disorders (p = 0.001) and PTSD avoidance and numbing symptoms (p = 0.02) at Time 1 were associated with an increasing pace of the epigenetic clock over time, per the Horvath (but not the Hannum) index of cellular aging. CONCLUSIONS: This is the first study to suggest that posttraumatic psychopathology is longitudinally associated with a quickened pace of the epigenetic clock. Results raise the possibility that accelerated cellular aging is a common biological consequence of stress-related psychopathology, which carries implications for identifying mechanisms of stress-related cellular aging and developing interventions to slow its pace.

10 Article Posttraumatic Stress Disorder Symptoms, Temperament, and the Pathway to Cellular Senescence. 2018

Connolly, Samantha L / Stoop, Tawni B / Logue, Mark W / Orr, Esther Hana / De Vivo, Immaculata / Miller, Mark W / Wolf, Erika J. ·Psychology Service, VA Boston Healthcare System, Boston, Massachusetts, USA. · National Center for PTSD at VA Boston Healthcare System, Boston, Massachusetts, USA. · Department of Psychiatry, Boston University School of Medicine, Boston, Massachusetts, USA. · Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. · Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA. ·J Trauma Stress · Pubmed #30338579.

ABSTRACT: Traumatic stress is thought to be associated with shortened telomere length (TL) in leukocytes, an age-related marker of increased risk for cellular senescence, although findings thus far have been mixed. We assessed associations between posttraumatic stress disorder (PTSD) symptom severity, temperament, and TL in a sample of 453 White, non-Hispanic, middle-aged, trauma-exposed male and female veterans and civilians. Given that prior research has suggested an association between PTSD and accelerated cellular age, we also examined associations between TL and an index of accelerated cellular age derived from DNA methylation data (DNAm age). Analyses revealed that, controlling for chronological age, PTSD was not directly associated with TL but rather this association was moderated by age, β = -.14, p = .003, ΔR

11 Article Stress-Generative Effects of Posttraumatic Stress Disorder: Transactional Associations Between Posttraumatic Stress Disorder and Stressful Life Events in a Longitudinal Sample. 2018

Maniates, Hannah / Stoop, Tawni B / Miller, Mark W / Halberstadt, Lisa / Wolf, Erika J. ·National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, Massachusetts, USA. · Department of Psychiatry, Boston University School of Medicine, Boston, Massachusetts, USA. · Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia, USA. ·J Trauma Stress · Pubmed #29630742.

ABSTRACT: Longitudinal studies have demonstrated transactional associations between psychopathology and stressful life events (SLEs), such that psychopathology predicts the occurrence of new SLEs, and SLEs in turn predict increasing symptom severity. The association between posttraumatic stress disorder (PTSD), specifically, and stress generation remains unclear. This study used temporally sequenced data from 116 veterans (87.9% male) to examine whether PTSD symptoms predicted new onset SLEs, and if these SLEs were associated with subsequent PTSD severity. The SLEs were objectively rated, using a clinician-administered interview and consensus-rating approach, to assess the severity, frequency, and personal dependence (i.e., if the event was due to factors that were independent of or dependent on the individual) of new-onset SLEs. A series of mediation models were tested, and results provided evidence for moderated mediation whereby baseline PTSD severity robustly predicted personally dependent SLEs, B = 0.03, p = .006, and dependent SLEs predicted increases in follow-up PTSD symptom severity, B = -0.04, p = .003, among participants with relatively lower baseline PTSD severity. After we controlled for baseline PTSD severity, personality traits marked by low constraint (i.e., high impulsivity) were also associated with an increased number of dependent SLEs. Our results provide evidence for a stress-generative role of PTSD and highlight the importance of developing interventions aimed at reducing the occurrence of personally dependent stressors.

12 Article Traumatic stress and accelerated DNA methylation age: A meta-analysis. 2018

Wolf, Erika J / Maniates, Hannah / Nugent, Nicole / Maihofer, Adam X / Armstrong, Don / Ratanatharathorn, Andrew / Ashley-Koch, Allison E / Garrett, Melanie / Kimbrel, Nathan A / Lori, Adriana / Va Mid-Atlantic Mirecc Workgroup, ? / Aiello, Allison E / Baker, Dewleen G / Beckham, Jean C / Boks, Marco P / Galea, Sandro / Geuze, Elbert / Hauser, Michael A / Kessler, Ronald C / Koenen, Karestan C / Miller, Mark W / Ressler, Kerry J / Risbrough, Victoria / Rutten, Bart P F / Stein, Murray B / Ursano, Robert J / Vermetten, Eric / Vinkers, Christiaan H / Uddin, Monica / Smith, Alicia K / Nievergelt, Caroline M / Logue, Mark W. ·National Center for PTSD at VA Boston Healthcare System, United States; Department of Psychiatry, Boston University School of Medicine, United States. Electronic address: erika.wolf@va.gov. · National Center for PTSD at VA Boston Healthcare System, United States. · Bradley Hasbro Children's Research Center, Rhode Island Hospital, United States; Departments of Psychiatry and Human Behavior and Pediatrics, Brown Medical School, United States. · University of California San Diego, Department of Psychiatry, United States. · University of Illinois Urbana-Champaign, Carl R. Woese Institute for Genomic Biology, United States. · Columbia University, Department of Epidemiology, United States. · Duke Molecular Physiology Institute, Duke University School of Medicine, United States. · Department of Psychiatry & Behavioral Sciences, Duke University Medical Center, United States. · Department of Psychiatry & Behavioral Sciences, Duke University Medical Center, United States; VA Mid-Atlantic, Mental Illness Research, Education, and Clinical Center, United States; Durham VA Medical Center, United States. · Department of Psychiatry and Behavioral Sciences, Emory University, United States. · VA Mid-Atlantic, Mental Illness Research, Education, and Clinical Center, United States. · Department of Epidemiology, University of North Carolina at Chapel Hill Gillings School of Global Public Health, United States. · University of California San Diego, Department of Psychiatry, United States; Veterans Affairs San Diego Healthcare System, United States; Veterans Affairs Center of Excellence for Stress and Mental Health, United States. · University Medical Center Utrecht, Brain Center Rudolf Magnus, Department of Psychiatry, Utrecht, The Netherlands. · Boston University School of Public Health, United States. · University Medical Center Utrecht, Brain Center Rudolf Magnus, Department of Psychiatry, Utrecht, The Netherlands; Ministry of Defence, Military Mental Healthcare, Utrecht, The Netherlands. · Harvard Medical School, Department of Health Care Policy, United States. · Harvard T.H. Chan School of Public Health, Department of Epidemiology, United States; Massachusetts General Hospital, Psychiatric and Neurodevelopmental Genetics Unit, Center for Human Genetic Research, and Department of Psychiatry, United States. · National Center for PTSD at VA Boston Healthcare System, United States; Department of Psychiatry, Boston University School of Medicine, United States. · Department of Psychiatry, Harvard Medical School and McLean Hospital, Belmont, MA, United States. · School for Mental Health and Neuroscience and the European Graduate School of Neuroscience (EURON), Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, Maastricht, The Netherlands. · University of California San Diego, Department of Psychiatry, United States; Veterans Affairs San Diego Healthcare System, United States; University of California San Diego, Department of Family Medicine and Public Health, United States. · Center for the Study of Traumatic Stress, Department of Psychiatry, Uniformed Services University of the Health Sciences, United States. · University Medical Center Utrecht, Brain Center Rudolf Magnus, Department of Psychiatry, Utrecht, The Netherlands; Ministry of Defence, Military Mental Healthcare, Utrecht, The Netherlands; Arq Psychotrauma Expert Group, The Netherlands. · University of Illinois Urbana-Champaign, Carl R. Woese Institute for Genomic Biology, United States; University of Illinois Urbana-Champaign, Department of Psychology, United States. · Department of Psychiatry and Behavioral Sciences, Emory University, United States; Department of Gynecology and Obstetrics, Emory University, United States. · National Center for PTSD at VA Boston Healthcare System, United States; Department of Psychiatry, Boston University School of Medicine, United States; Biomedical Genetics, Boston University School of Medicine, United States. ·Psychoneuroendocrinology · Pubmed #29452766.

ABSTRACT: BACKGROUND: Recent studies examining the association between posttraumatic stress disorder (PTSD) and accelerated aging, as defined by DNA methylation-based estimates of cellular age that exceed chronological age, have yielded mixed results. METHODS: We conducted a meta-analysis of trauma exposure and PTSD diagnosis and symptom severity in association with accelerated DNA methylation age using data from 9 cohorts contributing to the Psychiatric Genomics Consortium PTSD Epigenetics Workgroup (combined N = 2186). Associations between demographic and cellular variables and accelerated DNA methylation age were also examined, as was the moderating influence of demographic variables. RESULTS: Meta-analysis of regression coefficients from contributing cohorts revealed that childhood trauma exposure (when measured with the Childhood Trauma Questionnaire) and lifetime PTSD severity evidenced significant, albeit small, meta-analytic associations with accelerated DNA methylation age (ps = 0.028 and 0.016, respectively). Sex, CD4T cell proportions, and natural killer cell proportions were also significantly associated with accelerated DNA methylation age (all ps < 0.02). PTSD diagnosis and lifetime trauma exposure were not associated with advanced DNA methylation age. There was no evidence of moderation of the trauma or PTSD variables by demographic factors. CONCLUSIONS: Results suggest that traumatic stress is associated with advanced epigenetic age and raise the possibility that cells integral to immune system maintenance and responsivity play a role in this. This study highlights the need for additional research into the biological mechanisms linking traumatic stress to accelerated DNA methylation age and the importance of furthering our understanding of the neurobiological and health consequences of PTSD.

13 Article A classical twin study of PTSD symptoms and resilience: Evidence for a single spectrum of vulnerability to traumatic stress. 2018

Wolf, Erika J / Miller, Mark W / Sullivan, Danielle R / Amstadter, Ananda B / Mitchell, Karen S / Goldberg, Jack / Magruder, Kathryn M. ·National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA. · Department of Psychiatry, Boston University School of Medicine, Boston, MA, USA. · Department of Psychiatry and School of Medicine, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA. · Seattle Epidemiologic Research and Information Center, VA Puget Sound Health Care System, Seattle, WA, USA. · Department of Epidemiology, University of Washington, Seattle, WA, USA. · Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, SC, USA. ·Depress Anxiety · Pubmed #29283198.

ABSTRACT: BACKGROUND: To examine shared genetic and environmental risk factors across PTSD symptoms and resilience. METHODS: Classical twin study of 2010-2012 survey data conducted among 3,318 male twin pairs in the Vietnam Era Twin Registry. Analyses included: (a) estimates of genetic and environmental influences on PTSD symptom severity (as measured by the PTSD Checklist) and resilience (assessed with the Connor-Davidson Resilience Scale-10); (b) development of a latent model of traumatic stress, spanning both PTSD and resilience; and (c) estimates of genetic and environmental influences on this spectrum. RESULTS: The heritability of PTSD was 49% and of resilience was 25%. PTSD and resilience were correlated at r = -.59, and 59% of this correlation was attributable to a single genetic factor, whereas the remainder was due to a single non-shared environment factor. Resilience was also influenced by common and unique environmental factors not shared with PTSD, but there was no genetic factor specific to resilience. Confirmatory factor analysis supported the Development of a revised phenotype reflecting the broader dimension of traumatic stress, with biometric models suggesting increased heritability (66%) of this spectrum compared to PTSD or resilience individually. CONCLUSIONS: Genetic factors contribute to a single spectrum of traumatic stress reflecting resilience at one end and high symptom severity at the other. This carries implications for phenotype refinement in the search for molecular genetic markers of trauma-related psychopathology. Rather than focusing only on genetic risk for PTSD, molecular genetics research may benefit from evaluation of the broader spectrum of traumatic stress.

14 Article Accelerated DNA Methylation Age: Associations With Posttraumatic Stress Disorder and Mortality. 2018

Wolf, Erika J / Logue, Mark W / Stoop, Tawni B / Schichman, Steven A / Stone, Annjanette / Sadeh, Naomi / Hayes, Jasmeet P / Miller, Mark W. ·From the National Center for PTSD (Wolf, Logue, Sadeh, Hayes, Miller), Behavioral Science Division, VA Boston Healthcare System · Department of Psychiatry (Wolf, Sadeh, Hayes, Miller), Boston University School of Medicine · Biomedical Genetics (Logue), Boston University School of Medicine · Department of Biostatistics (Logue), Boston University School of Public Health · Research Service (Stoop), VA Boston Healthcare System · and Pharmacogenomics Analysis Laboratory (Schichman, Stone), Research Service, Central Arkansas Veterans Healthcare System, Boston, Massachusetts. ·Psychosom Med · Pubmed #29271864.

ABSTRACT: OBJECTIVE: Recently developed indices of cellular age based on DNA methylation (DNAm) data, referred to as DNAm age, are being used to study factors that influence the rate of aging and the health correlates of these metrics of the epigenetic clock. This study evaluated associations between trauma exposure, posttraumatic stress disorder (PTSD) symptoms, and accelerated versus decelerated DNAm age among military veterans. We also examined whether accelerated DNAm age predicted mortality over the course of a 6.5-year medical record review period. METHODS: Three hundred thirty-nine genotype-confirmed white, non-Hispanic, middle-aged, trauma-exposed veterans underwent psychiatric assessment and genome-wide DNAm analysis. DNAm age was calculated using a previously validated algorithm. Medical records were available for a subset of 241 veterans and were reviewed approximately 6.5 years after DNA collection and PTSD assessment. RESULTS: PTSD hyperarousal symptoms were associated with accelerated DNAm age (β = 0.20, p = .009) but trauma exposure and total PTSD severity were not. Accelerated DNAm age was also associated with 13% increased risk for all-cause mortality (hazard ratio = 1.13, 95% confidence interval = 1.01-1.26) during the medical record review period. CONCLUSIONS: Findings of this study replicate the association between PTSD and accelerated DNAm age and suggest that this effect may be specific to the hyperarousal symptom cluster. Results point to the potential utility of DNAm age algorithms for identifying individuals who are aging at an accelerated rate and for determining the factors that influence this process.

15 Article Smaller Hippocampal Volume in Posttraumatic Stress Disorder: A Multisite ENIGMA-PGC Study: Subcortical Volumetry Results From Posttraumatic Stress Disorder Consortia. 2018

Logue, Mark W / van Rooij, Sanne J H / Dennis, Emily L / Davis, Sarah L / Hayes, Jasmeet P / Stevens, Jennifer S / Densmore, Maria / Haswell, Courtney C / Ipser, Jonathan / Koch, Saskia B J / Korgaonkar, Mayuresh / Lebois, Lauren A M / Peverill, Matthew / Baker, Justin T / Boedhoe, Premika S W / Frijling, Jessie L / Gruber, Staci A / Harpaz-Rotem, Ilan / Jahanshad, Neda / Koopowitz, Sheri / Levy, Ifat / Nawijn, Laura / O'Connor, Lauren / Olff, Miranda / Salat, David H / Sheridan, Margaret A / Spielberg, Jeffrey M / van Zuiden, Mirjam / Winternitz, Sherry R / Wolff, Jonathan D / Wolf, Erika J / Wang, Xin / Wrocklage, Kristen / Abdallah, Chadi G / Bryant, Richard A / Geuze, Elbert / Jovanovic, Tanja / Kaufman, Milissa L / King, Anthony P / Krystal, John H / Lagopoulos, Jim / Bennett, Maxwell / Lanius, Ruth / Liberzon, Israel / McGlinchey, Regina E / McLaughlin, Katie A / Milberg, William P / Miller, Mark W / Ressler, Kerry J / Veltman, Dick J / Stein, Dan J / Thomaes, Kathleen / Thompson, Paul M / Morey, Rajendra A. ·National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, Massachusetts; Department of Psychiatry, Boston University School of Medicine, Boston, Massachusetts; Department of Biomedical Genetics, Boston University School of Medicine, Boston, Massachusetts; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. · Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, Georgia. · Imaging Genetics Center, Mary and Mark Stevens Institute for Neuroimaging and Informatics, Keck School of Medicine, University of Southern California, Marina del Rey, California. · Mid-Atlantic Mental Illness Research, Education and Clinical Center, Durham VA Medical Center, Durham, North Carolina; Duke-UNC Brain Imaging and Analysis Center, Duke University, Durham, North Carolina. · National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, Massachusetts; Department of Psychiatry, Boston University School of Medicine, Boston, Massachusetts. · Department of Psychiatry, University of Western Ontario, London, Ontario, Canada. · Department of Psychiatry, University of Cape Town, Cape Town, South Africa. · Brain Imaging Center, Academic Medical Center, Amsterdam, the Netherlands. · Brain Dynamics Centre, Westmead Institute for Medical Research, Sydney, Australia. · Department of Psychiatry, Harvard Medical School, Boston, Massachusetts; McLean Hospital, Harvard University, Belmont, Massachusetts. · Department of Psychology, University of Washington, Seattle, Washington. · McLean Hospital, Harvard University, Belmont, Massachusetts. · Department of Psychiatry, VU University Medical Center, Amsterdam, the Netherlands. · Department of Psychiatry, Academic Medical Center, Amsterdam, the Netherlands. · Clinical Neuroscience Division, VA National Center for PTSD, VA Connecticut HealthCare System, West Haven, Connecticut; Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut. · Clinical Neuroscience Division, VA National Center for PTSD, VA Connecticut HealthCare System, West Haven, Connecticut; Interdepartmental Neuroscience Program, Yale University, New Haven, Connecticut. · Department of Psychology, John Jay College of Criminal Justice, City University of New York, New York, New York; Graduate Center, City University of New York, New York, New York. · Department of Psychiatry, Academic Medical Center, Amsterdam, the Netherlands; Department of Psychiatry, Arq National Trauma Center, Diemen, the Netherlands. · Neuroimaging Research for Veterans Center, VA Boston Healthcare System, Boston, Massachusetts; Department of Radiology, Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts. · Department of Psychology and Neuroscience, University of North Carolina, Chapel Hill, North Carolina. · Neuroimaging Research for Veterans Center, VA Boston Healthcare System, Boston, Massachusetts; Department of Psychological and Brain Sciences, University of Delaware, Newark, Delaware. · Department of Psychiatry, University of Toledo, Toledo, Ohio. · Department of Psychology, University of New South Wales, Sydney, Australia. · Brain Center Rudolf Magnus, University Medical Center, Utrecht, the Netherlands. · Department of Psychiatry, University of Michigan, Ann Arbor, Michigan. · Neuroimaging Brain & Mind Research Institute, University of Sydney, Sydney, Australia. · National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, Massachusetts; Department of Psychiatry, University of Western Ontario, London, Ontario, Canada. · Translational Research Center for TBI and Stress Disorders, VA Boston Healthcare System, Boston, Massachusetts; Geriatric Research, Educational and Clinical Center, VA Boston Healthcare System, Boston, Massachusetts; Department of Psychiatry, Harvard Medical School, Boston, Massachusetts. · McLean Hospital, Harvard University, Belmont, Massachusetts; Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, Georgia. · Mid-Atlantic Mental Illness Research, Education and Clinical Center, Durham VA Medical Center, Durham, North Carolina; Duke-UNC Brain Imaging and Analysis Center, Duke University, Durham, North Carolina; Department of Psychiatry and Behavioral Sciences, Duke University, Durham, North Carolina. Electronic address: rajendra.morey@duke.edu. ·Biol Psychiatry · Pubmed #29217296.

ABSTRACT: BACKGROUND: Many studies report smaller hippocampal and amygdala volumes in posttraumatic stress disorder (PTSD), but findings have not always been consistent. Here, we present the results of a large-scale neuroimaging consortium study on PTSD conducted by the Psychiatric Genomics Consortium (PGC)-Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) PTSD Working Group. METHODS: We analyzed neuroimaging and clinical data from 1868 subjects (794 PTSD patients) contributed by 16 cohorts, representing the largest neuroimaging study of PTSD to date. We assessed the volumes of eight subcortical structures (nucleus accumbens, amygdala, caudate, hippocampus, pallidum, putamen, thalamus, and lateral ventricle). We used a standardized image-analysis and quality-control pipeline established by the ENIGMA consortium. RESULTS: In a meta-analysis of all samples, we found significantly smaller hippocampi in subjects with current PTSD compared with trauma-exposed control subjects (Cohen's d = -0.17, p = .00054), and smaller amygdalae (d = -0.11, p = .025), although the amygdala finding did not survive a significance level that was Bonferroni corrected for multiple subcortical region comparisons (p < .0063). CONCLUSIONS: Our study is not subject to the biases of meta-analyses of published data, and it represents an important milestone in an ongoing collaborative effort to examine the neurobiological underpinnings of PTSD and the brain's response to trauma.

16 Article CRP polymorphisms and DNA methylation of the AIM2 gene influence associations between trauma exposure, PTSD, and C-reactive protein. 2018

Miller, M W / Maniates, H / Wolf, E J / Logue, M W / Schichman, S A / Stone, A / Milberg, W / McGlinchey, R. ·National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, MA, USA; Department of Psychiatry, Boston University School of Medicine, Boston, MA, USA. Electronic address: mark.miller5@va.gov. · National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, MA, USA. · National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, MA, USA; Department of Psychiatry, Boston University School of Medicine, Boston, MA, USA. · National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, MA, USA; Department of Biomedical Genetics, Boston University School of Medicine, Boston, MA, USA; Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA. · Pharmacogenomics Analysis Laboratory, Research Service, Central Arkansas Veterans Healthcare System, Little Rock, AR, USA. · Translational Research Center for TBI and Stress Disorders and Geriatric Research, Educational and Clinical Center, VA Boston Healthcare System, Boston, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA. ·Brain Behav Immun · Pubmed #28867284.

ABSTRACT: BACKGROUND: Recent studies have implicated inflammatory processes in the pathophysiology of posttraumatic stress disorder (PTSD). C-reactive protein (CRP) is a widely-used measure of peripheral inflammation, but little is known about the genetic and epigenetic factors that influence blood levels of C-reactive protein (CRP) in individuals with PTSD. METHODS: Participants were 286 U.S. military veterans of post-9/11 conflicts (57% with current PTSD). Analyses focused on single nucleotide polymorphisms (SNPs) in the CRP gene and DNA methylation at cg10636246 in AIM2-a locus recently linked to CRP levels through results from a large-scale epigenome-wide association study. RESULTS: PTSD was positively correlated with serum CRP levels with PTSD cases more likely to have CRP levels in the clinically-elevated range compared to those without a PTSD diagnosis. Multivariate analyses that controlled for white blood cell proportions, genetic principal components, age and sex, showed this association to be mediated by methylation at the AIM2 locus. rs3091244, a functional SNP in the CRP promoter region, moderated the association between lifetime trauma exposure and current PTSD severity. Analyses also revealed that the top SNPs from the largest genome-wide association study of CRP conducted to date (rs1205 and rs2794520) significantly interacted with PTSD to influence CRP levels. CONCLUSIONS: These findings provide new insights into genetic and epigenetic mechanisms of inflammatory processes in the pathophysiology of PTSD and point to new directions for biomarker identification and treatment development for patients with PTSD.

17 Article A comparison of ICD-11 and DSM criteria for posttraumatic stress disorder in two national samples of U.S. military veterans. 2017

Wisco, Blair E / Marx, Brian P / Miller, Mark W / Wolf, Erika J / Krystal, John H / Southwick, Steven M / Pietrzak, Robert H. ·University of North Carolina at Greensboro, Psychology Department, PO Box 26170, Greensboro, NC 27402, United States. Electronic address: bewisco@uncg.edu. · National Center for PTSD, VA Boston Healthcare System/Boston University School of Medicine, United States. · National Center for PTSD, VA Connecticut Healthcare System/Yale University, United States. ·J Affect Disord · Pubmed #28715723.

ABSTRACT: BACKGROUND: The proposed ICD-11 criteria for posttraumatic stress disorder (PTSD) differ substantially from the DSM-5. ICD-11 eliminated several PTSD symptoms thought to be nonspecific, with the goal of reducing psychiatric comorbidities. However, this change also results in a narrower PTSD definition that may fail to capture individuals with clinically significant PTSD. The purpose of the current study was to compare prevalence and psychiatric comorbidities of DSM (IV/5) and ICD-11 PTSD. METHODS: We evaluated concordance between DSM (IV/5) and ICD-11 PTSD diagnoses in a web survey of two nationally representative samples of U.S. military veterans (ns = 3517 and 1484). Lifetime and past-month PTSD symptoms were assessed with the DSM-IV-based PTSD Checklist-Specific Stressor version and the DSM-5-based PTSD Checklist-5. Psychiatric comorbidities were assessed using MINI Neuropsychiatric Interview modules. RESULTS: A significantly greater proportion of veterans met criteria for lifetime and past-month PTSD under DSM-IV/5 than under ICD-11. 21.8-35.9% of those who met criteria under DSM IV/5 did not meet under ICD-11, whereas only 2.4-7.1% of those who met under ICD-11 did not meet under DSM-IV/5. Psychiatric comorbidities did not significantly differ between DSM-IV/5 and ICD-11. LIMITATIONS: This study relied upon self-report measures of PTSD, distress/impairment, and psychiatric comorbidities. CONCLUSIONS: The proposed ICD-11 criteria identify fewer PTSD cases than DSM-IV/5 without reducing psychiatric comorbidities. Veterans with clinically significant PTSD symptoms may not meet ICD-11 PTSD criteria, possibly affecting eligibility for healthcare, disability, and other services. The ICD-11 criteria could be revised to capture more PTSD cases before ICD-11 is published in 2018.

18 Article Contributions of polygenic risk for obesity to PTSD-related metabolic syndrome and cortical thickness. 2017

Wolf, Erika J / Miller, Danielle R / Logue, Mark W / Sumner, Jennifer / Stoop, Tawni B / Leritz, Elizabeth C / Hayes, Jasmeet P / Stone, Annjanette / Schichman, Steven A / McGlinchey, Regina E / Milberg, William P / Miller, Mark W. ·National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, MA, United States; Department of Psychiatry, Boston University School of Medicine, Boston, MA, United States. Electronic address: erika.wolf@va.gov. · National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, MA, United States; Department of Psychiatry, Boston University School of Medicine, Boston, MA, United States. · National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, MA, United States; Biomedical Genetics, Boston University School of Medicine, Boston, MA, United States; Department of Biostatistics, Boston University School of Public Health, Boston, MA, United States. · Center for Behavioral Cardiovascular Health, Columbia University Medical Center, NY, NY, United States. · Research Service, VA Boston Healthcare System, Boston, MA, United States. · Neuroimaging Research for Veterans Center, VA Boston Healthcare System, Boston, MA, United States; Geriatric Research Educational and Clinical Center and Translational Research Center for TBI and Stress Disorders, VA Boston Healthcare System, Boston, MA, United States; Department of Psychiatry, Harvard Medical School, Boston, MA, United States. · National Center for PTSD, Behavioral Science Division, VA Boston Healthcare System, Boston, MA, United States; Department of Psychiatry, Boston University School of Medicine, Boston, MA, United States; Neuroimaging Research for Veterans Center, VA Boston Healthcare System, Boston, MA, United States. · Pharmacogenomics Analysis Laboratory, Research Service, Central Arkansas Veterans Healthcare System, United States. · Geriatric Research Educational and Clinical Center and Translational Research Center for TBI and Stress Disorders, VA Boston Healthcare System, Boston, MA, United States; Department of Psychiatry, Harvard Medical School, Boston, MA, United States. ·Brain Behav Immun · Pubmed #28579519.

ABSTRACT: BACKGROUND: Research suggests that posttraumatic stress disorder (PTSD) is associated with metabolic syndrome (MetS) and that PTSD-associated MetS is related to decreased cortical thickness. However, the role of genetic factors in these associations is unclear. This study evaluated contributions of polygenic obesity risk and PTSD to MetS and of MetS and polygenic obesity risk to cortical thickness. METHODS: 196 white, non-Hispanic veterans of the wars in Iraq and Afghanistan underwent clinical diagnostic interviews, physiological assessments, and genome-wide genotyping; 168 also completed magnetic resonance imaging scans. Polygenic risk scores (PRSs) for obesity were calculated from results of a prior genome-wide association study (Speliotes et al., 2010) and PTSD and MetS severity factor scores were obtained. RESULTS: Obesity PRS (β=0.15, p=0.009) and PTSD (β=0.17, p=0.005) predicted MetS and interacted such that the association between PTSD and MetS was stronger in individuals with greater polygenic obesity risk (β=0.13, p=0.02). Whole-brain vertex-wise analyses suggested that obesity PRS interacted with MetS to predict decreased cortical thickness in left rostral middle frontal gyrus (β=-0.40, p<0.001). CONCLUSIONS: Results suggest that PTSD, genetic variability, and MetS are related in a transactional fashion wherein obesity genetic risk increases stress-related metabolic pathology, and compounds the ill health effects of MetS on the brain. Genetic proclivity towards MetS should be considered in PTSD patients when prescribing psychotropic medications with adverse metabolic profiles. Results are consistent with a growing literature suggestive of PTSD-related accelerated aging.

19 Article Posttraumatic stress disorder symptom severity is associated with reduced default mode network connectivity in individuals with elevated genetic risk for psychopathology. 2017

Miller, Danielle R / Logue, Mark W / Wolf, Erika J / Maniates, Hannah / Robinson, Meghan E / Hayes, Jasmeet P / Stone, Annjanette / Schichman, Steven / McGlinchey, Regina E / Milberg, William P / Miller, Mark W. ·National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA. · Department of Psychiatry, Boston University School of Medicine, Boston, MA, USA. · Biomedical Genetics, Boston University School of Medicine, Boston, MA, USA. · Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA. · Neuroimaging Research for Veterans Center, VA Boston Healthcare System, Boston, MA, USA. · Department of Neurology, Boston University School of Medicine, Boston, MA, USA. · Translational Research Center for TBI and Stress Disorders, VA Boston Healthcare System, Boston, MA, USA, USA. · Pharmacogenomics Analysis Laboratory, Research Service, Central Arkansas Veterans Healthcare System, Little Rock, AR, USA. · Geriatric Research, Educational, and Clinical Center, VA Boston Healthcare System, Boston, MA, USA, USA. · Department of Psychiatry, Harvard Medical School, Boston, MA, USA. ·Depress Anxiety · Pubmed #28494120.

ABSTRACT: BACKGROUND: Accumulating evidence suggests that posttraumatic stress disorder (PTSD) is associated with disrupted default mode network (DMN) connectivity, but findings across studies have not been uniform. Individual differences in relevant genes may account for some of the reported variability in the relationship between DMN connectivity and PTSD. In this study, we investigated this possibility using genome-wide association study (GWAS) derived polygenic risk scores (PRSs) for relevant psychiatric traits. We hypothesized that the association between PTSD and DMN connectivity would be moderated by genetic risk for one or more psychiatric traits such that individuals with elevated polygenic risk for psychopathology and severe PTSD would exhibit disrupted DMN connectivity. METHODS: Participants were 156 white, non-Hispanic veterans of the wars in Iraq and Afghanistan who were genotyped and underwent resting state functional magnetic resonance imaging and clinical assessment. PRSs for neuroticism, anxiety, major depressive disorder, and cross-disorder risk (based on five psychiatric disorders) were calculated using summary statistics from published large-scale consortia-based GWASs. RESULTS: Cross-disorder polygenic risk influenced the relationship between DMN connectivity and PTSD symptom severity such that individuals at greater genetic risk showed a significant negative association between PTSD symptom severity and connectivity between the posterior cingulate cortex and right middle temporal gyrus. Polygenic risk for neuroticism, anxiety, and major depressive disorder did not influence DMN connectivity directly or through an interaction with PTSD. CONCLUSIONS: Findings illustrate the potential power of genome-wide PRSs to advance understanding of the relationship between PTSD and DMN connectivity, a putative neural endophenotype of the disorder.

20 Article Reckless Self-Destructive Behavior and PTSD in Veterans: The Mediating Role of New Adverse Events. 2017

Lusk, Joanna D / Sadeh, Naomi / Wolf, Erika J / Miller, Mark W. ·National Center for PTSD at VA Boston Healthcare System, Boston, Massachusetts, USA. · Department of Psychiatry, Boston University School of Medicine, Boston, Massachusetts, USA. · Department of Psychological and Brain Sciences, University of Delaware, Newark, Delaware, USA. ·J Trauma Stress · Pubmed #28471014.

ABSTRACT: The addition of self-destructive and reckless behavior as a symptom of posttraumatic stress disorder (PTSD) in DSM-5 has stimulated renewed interest in understanding relationships between these behaviors and trauma-related psychopathology. This study examined the relationship between reckless and self-destructive behaviors (RSDB), intervening exposure to new adverse events, and later PTSD severity in a sample of trauma-exposed veterans. At baseline, participants were assessed for RSDB (past 5 years) and current PTSD severity (N = 222). PTSD severity was then reassessed approximately 4 years later (N = 148). Overall, RSDB were reported by 74.4% of the sample, with 61.3% engaging in multiple forms of RSDB. The most commonly endorsed behaviors included alcohol/drug abuse (42.8%), driving while intoxicated (29.4%), gambling (24.7%), and aggression (23.1%). There was a positive correlation between RSDB and PTSD severity at both the baseline (r = .16, p = .031) and follow-up assessment (r = .24, p = .005). Path models indicated that exposure to new adverse events fully mediated the effect of Time 1 RSDB on PTSD symptoms at Time 2 (indirect association: β = .05, p = .046). Results suggest that RSDB are common among trauma-exposed veterans and may perpetuate PTSD symptoms by increasing exposure to new adverse events.

21 Article COMT Val158Met polymorphism moderates the association between PTSD symptom severity and hippocampal volume. 2017

Hayes, Jasmeet P / Logue, Mark W / Reagan, Andrew / Salat, David / Wolf, Erika J / Sadeh, Naomi / Spielberg, Jeffrey M / Sperbeck, Emily / Hayes, Scott M / McGlinchey, Regina E / Milberg, William P / Verfaellie, Mieke / Stone, Annjanette / Schichman, Steven A / Miller, Mark W. ·From the National Center for PTSD, VA Boston Healthcare System, Boston, Mass. (Hayes, Reagan, Wolf, Sadeh, Miller) · the Department of Psychiatry, Boston University School of Medicine, Boston, Mass. (Hayes, Wolf, Sadeh, Spielberg, Sperbeck, Hayes, Verfaellie, Miller) · the Neuroimaging Research for Veterans Center, VA Boston Healthcare System, Boston, Mass. (Hayes, Salat, Spielberg, Hayes) · the Research Service, VA Boston Healthcare System, Boston, Mass. (Logue) · the Biomedical Genetics, Boston University School of Medicine, Boston, Mass. (Logue) · the Department of Biostatistics, Boston University School of Public Health, Boston, Mass. (Logue) · the Memory Disorders Research Center, VA Boston Healthcare System, Boston, Mass. (Hayes, Verfaellie) · the Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Harvard University, Boston, Mass. (Salat) · the Harvard Medical School, Harvard University, Boston, Mass. (Salat) · the Translational Research Center for TBI and Stress Disorders and Geriatric Research, Educational and Clinical Center, VA Boston Healthcare System, Boston, Mass. (McGlinchey, Milberg) · the Department of Psychiatry, Harvard Medical School, Boston, Mass. (McGlinchey, Milberg) · the Pharmacogenomics Analysis Laboratory, Research Service, Central Arkansas Veterans Healthcare System, USA (Stone, Schichman). ·J Psychiatry Neurosci · Pubmed #28234210.

ABSTRACT: BACKGROUND: Memory-based alterations are among the hallmark symptoms of posttraumatic stress disorder (PTSD) and may be associated with the integrity of the hippocampus. However, neuroimaging studies of hippocampal volume in individuals with PTSD have yielded inconsistent results, raising the possibility that various moderators, such as genetic factors, may influence this association. We examined whether the catechol-O-methyltransferase (COMT) Val158Met polymorphism, which has previously been shown to be associated with hippocampal volume in healthy individuals, moderates the association between PTSD and hippocampal volume. METHODS: Recent war veterans underwent structural MRI on a 3 T scanner. We extracted volumes of the right and left hippocampus using FreeSurfer and adjusted them for individual differences in intracranial volume. We assessed PTSD severity using the Clinician-Administered PTSD Scale. Hierarchical linear regression was used to model the genotype (Val158Met polymorphism) × PTSD severity interaction and its association with hippocampal volume. RESULTS: We included 146 white, non-Hispanic recent war veterans (90% male, 53% with diagnosed PTSD) in our analyses. A significant genotype × PTSD symptom severity interaction emerged such that individuals with greater current PTSD symptom severity who were homozygous for the Val allele showed significant reductions in left hippocampal volume. LIMITATIONS: The direction of proposed effects is unknown, thus precluding definitive assessment of whether differences in hippocampal volume reflect a consequence of PTSD, a pre-existing characteristic, or both. CONCLUSION: Our findings suggest that the COMT polymorphism moderates the association between PTSD and hippocampal volume. These results highlight the role that the dopaminergic system has in brain structure and suggest a possible mechanism for memory disturbance in individuals with PTSD.

22 Article Longitudinal Associations between Posttraumatic Stress Disorder Severity and Personality Disorder Features among Female Rape Survivors. 2017

Bovin, Michelle J / Wolf, Erika J / Resick, Patricia A. ·VA National Center for PTSD, Boston, MA, USA; Boston University School of Medicine, Boston, MA, USA. · Duke University Medical Center , Durham, NC , USA. ·Front Psychiatry · Pubmed #28210229.

ABSTRACT: This study evaluated how change in posttraumatic stress disorder (PTSD) symptoms was associated with residualized change in comorbid personality disorder (PD) features and

23 Article Network models of DSM-5 posttraumatic stress disorder: Implications for ICD-11. 2017

Mitchell, Karen S / Wolf, Erika J / Bovin, Michelle J / Lee, Lewina O / Green, Jonathan D / Rosen, Raymond C / Keane, Terence M / Marx, Brian P. ·National Center for PTSD, VA Boston Healthcare System. · VA Boston Healthcare System, Research Service. · New England Research Institutes. ·J Abnorm Psychol · Pubmed #28191985.

ABSTRACT: Recent proposals for revisions to the 11th edition of the

24 Article The Dissociative Subtype of PTSD Scale: Initial Evaluation in a National Sample of Trauma-Exposed Veterans. 2017

Wolf, Erika J / Mitchell, Karen S / Sadeh, Naomi / Hein, Christina / Fuhrman, Isaac / Pietrzak, Robert H / Miller, Mark W. ·1 National Center for PTSD at VA Boston Healthcare System, Boston, MA, USA. · 2 Boston University School of Medicine, Boston, MA, USA. · 3 Boston VA Research Institute, Boston, MA, USA. · 4 National Center for PTSD at VA Connecticut Healthcare System, New Haven, CT, USA. · 5 Yale University School of Medicine, New Haven, CT, USA. ·Assessment · Pubmed #26603115.

ABSTRACT: The fifth edition of the Diagnostic and Statistical Manual includes a dissociative subtype of posttraumatic stress disorder, but no existing measures specifically assess it. This article describes the initial evaluation of a 15-item self-report measure of the subtype called the Dissociative Subtype of Posttraumatic Stress Disorder Scale (DSPS) in an online survey of 697 trauma-exposed military veterans representative of the U.S. veteran population. Exploratory factor analyses of the lifetime DSPS items supported the intended structure of the measure consisting of three factors reflecting derealization/depersonalization, loss of awareness, and psychogenic amnesia. Consistent with prior research, latent profile analyses assigned 8.3% of the sample to a highly dissociative class distinguished by pronounced symptoms of derealization and depersonalization. Overall, results provide initial psychometric support for the lifetime DSPS scales; additional research in clinical and community samples is needed to further validate the measure.

25 Article Probable Posttraumatic Stress Disorder in the US Veteran Population According to DSM-5: Results From the National Health and Resilience in Veterans Study. 2016

Wisco, Blair E / Marx, Brian P / Miller, Mark W / Wolf, Erika J / Mota, Natalie P / Krystal, John H / Southwick, Steven M / Pietrzak, Robert H. ·University of North Carolina at Greensboro, Department of Psychology, PO Box 26170, Greensboro, NC 27402. bewisco@uncg.edu. · Department of Psychology, University of North Carolina at Greensboro, Greensboro, North Carolina, USA. · National Center for PTSD, VA Boston Healthcare System and Department of Psychiatry, Boston University School of Medicine, Massachusetts, USA. · National Center for PTSD, VA Connecticut Healthcare System, and Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut, USA. ·J Clin Psychiatry · Pubmed #27631148.

ABSTRACT: OBJECTIVE: With the publication of DSM-5, important changes were made to the diagnostic criteria for posttraumatic stress disorder (PTSD), including the addition of 3 new symptoms. Some have argued that these changes will further increase the already high rates of comorbidity between PTSD and other psychiatric disorders. This study examined the prevalence of DSM-5 PTSD, conditional probability of PTSD given certain trauma exposures, endorsement of specific PTSD symptoms, and psychiatric comorbidities in the US veteran population. METHODS: Data were analyzed from the National Health and Resilience in Veterans Study (NHRVS), a Web-based survey of a cross-sectional, nationally representative, population-based sample of 1,484 US veterans, which was fielded from September through October 2013. Probable PTSD was assessed using the PTSD Checklist-5. RESULTS: The weighted lifetime and past-month prevalence of probable DSM-5 PTSD was 8.1% (SE = 0.7%) and 4.7% (SE = 0.6%), respectively. Conditional probability of lifetime probable PTSD ranged from 10.1% (sudden death of close family member or friend) to 28.0% (childhood sexual abuse). The DSM-5 PTSD symptoms with the lowest prevalence among veterans with probable PTSD were trauma-related amnesia and reckless and self-destructive behavior. Probable PTSD was associated with increased odds of mood and anxiety disorders (OR = 7.6-62.8, P < .001), substance use disorders (OR = 3.9-4.5, P < .001), and suicidal behaviors (OR = 6.7-15.1, P < .001). CONCLUSIONS: In US veterans, the prevalence of DSM-5 probable PTSD, conditional probability of probable PTSD, and odds of psychiatric comorbidity were similar to prior findings with DSM-IV-based measures; we found no evidence that changes in DSM-5 increase psychiatric comorbidity. Results underscore the high rates of exposure to both military and nonmilitary trauma and the high public health burden of DSM-5 PTSD and comorbid conditions in veterans.

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