Current Faculty

Degree Year Institution Field of Study
Ph.D. 1977 University of Maryland Medical School, MD Anatomy
M.S. 1972 Pennsylvania State University, PA Zoology
B.A. 1969 Wilkes University, PA Biology

POST-GRADUATE MEDICAL EDUCATION:
Specialty Year Institution
Post-Doctoral Fellow 1976 to 1980 NINCDS, NIH

Juanita Anders is internationally recognized as an expert in Photobiomodulation research and has served as invited Chair and Speaker globally. Her specialty is peripheral and central nervous system injury and repair mechanisms, and light tissue interactions. Dr. Anders received her Ph.D. in Anatomy from the University of Maryland Medical School then joined the National Institutes of Health in the Laboratory of Neuropathology and Neuroanatomical Sciences, NINDS. She is affiliated with the Uniformed Services University of the Health Sciences as a Professor of Anatomy, Physiology and Genetics and Professor of Neuroscience. Dr. Anders serves on the Executive Councils and Scientific Advisory Boards of numerous international laser conferences. She is the past president of the North American Association of Laser Therapy, a founding member of the International Academy of Laser Medicine and Surgery, and Past President of the American Society of Lasers in Medicine and Surgery. She has recently been appointed as a board member of the International Society of Lasers in Medicine and Surgery and currently serves as the Director of the Optical Society of America Photobiomodulation Technical Group. She is a Senior Editor of Photomedicine and Laser Surgery, Associate Editor of Lasers in Surgery and Medicine, Associate Editor of Lasers in Medical Science, and on the editorial board of Physiotherapy Practice and Research and has published over 70 peer reviewed articles.

1987 University of North Carolina, Chapel Hill, NC Ph.D. in Neurobiology
1982 University of Rochester, Rochester, NY B.S. in Neurosciences

Dr. Armstrong’s primary academic appointment is as Professor of Anatomy, Physiology, and Genetics in the F. Edward Hebert School of Medicine at USU. Dr. Armstrong holds secondary appointments in the Neuroscience and the Molecular and Cell Biology Graduate Programs. Dr. Armstrong received the faculty award for Outstanding Graduate Biomedical Educator from the School of Medicine in 2002. She served as Director of the USU Neuroscience Graduate Program from 2002-2008 before stepping down to establish the Center for Neuroscience and Regenerative Medicine (CNRM). The CNRM is a collaborative intramural research program of the Uniformed Services University of the Health Sciences (USU) with the National Institutes of Health (NIH) and the Walter Reed National Military Medical Center (WRNMMC). The CNRM focus is pre-clinical through clinical research to promote recovery from traumatic brain injury and to improve psychological health in combat casualties cared for at WRNMMC. Dr. Armstrong served as the Director of the CNRM from 2008-2017 and now serves as the CNRM Director of Translational Research.
Dr. Armstrong teaches in the first year medical student module on the nervous system and in several graduate student courses. Dr. Armstrong’s laboratory focuses on mechanisms of damage and repair in the brain and spinal cord. This work employs diverse research approaches, from molecular techniques to neuroimaging, to address ways to improve neuroregeneration and repair capacity in the CNS. Research efforts in her laboratory have been funded through peer-reviewed competitive awards from the NIH, the National Multiple Sclerosis Foundation, and the Department of Defense.
Dr. Armstrong’s research program has focused on cellular and molecular mechanisms of neuroregeneration. This work has taken from developmental studies and applied the techniques and approaches to examine repair after disease or injury. More specifically, her lab has extensive experience in white matter injury in multiple sclerosis models and in single and repetitive closed head injury models of mild traumatic brain injury.
Her research team uses diverse approaches including genetic mouse models, neural stem cell culture, immunohistochemistry, in situ hybridization, fluorescence imaging, magnetic resonance imaging and behavioral assessments. Our philosophy is that combining multiple independent techniques will result in more in-depth understanding and improved translational potential. Our work has also utilized collaborations to include analysis of human neuropathological specimens to validate aspects of our animal model studies.

Ph.D. (Anatomy), University of Pennsylvania, Philadelphia, PA.
B.A. (Biology), Goucher College, Towson, MD.

The amygdala, an almond-shaped structure in the midtemporal lobe, plays a central role in emotional behavior, as well as in modulating cognitive functions. Thus, the amygdala is a key component of the brain's neuronal networks that determine the emotional significance of external -and internal- events. Via reciprocal connections with the prefrontal cortex, the amygdala provides a neurobiological substrate through which emotions affect cognition (and vice versa). Via reciprocal connections with the hippocampus, as well as with other cortical and subcortical areas, the amygdala modulates memory functions, and mediates certain forms of memory. Furthermore, via efferent pathways to the hypothalamus, the amygdala can trigger the autonomic and endocrine cascades associated with the response to a stressful event. It is not surprising therefore, that many emotional/psychiatric disorders are associated with dysfunction of the amygdala. For example, anxiety disorders are associated with a hyperactive and/or hyperexcitable amygdala. One goal of the research program in our laboratory is to understand the mechanisms regulating neuronal excitability in the amygdala, and the alterations in these mechanisms in anxiety disorders. As the GABAergic and glutamatergic system are the primary determinants of neuronal excitability in the brain, we are using electrophysiological techniques (whole-cell patch-clamp, intracellular and field potential recordings), as well as molecular methods, to study the modulation of GABAergic and glutamatergic synaptic transmission in the amygdala of normal and fear-conditioned rats and mice. We also study plasticity of glutamatergic synaptic transmission (Long-Term Potentiation, LTP) in these animals, as LTP is considered to be the cellular mechanism for acquiring and consolidating information, and therefore alterations in synaptic plasticity can have a profound effect on the function of a brain region.

In addition to its role in emotional disorders, the amygdala also plays a central role in epilepsy. The basolateral nucleus of the amygdala (BLA), in particular, is highly prone to generating seizure activity, and, in many models of epilepsy, it is the focal point from where epileptic activity is spread to other brain areas, culminating in status epilepticus. The second research goal in our laboratory is to understand the role of the amygdala in epileptogenesis. Epileptogenesis is the process whereby, after an acute brain insult, such as traumatic brain injury, progressive pathophysiological alterations in neuronal networks occur that lead to the development of epilepsy. We recently identified an important mechanism regulating neuronal excitability and epileptic activity in BLA. We demonstrated that, in the rat BLA, kainate receptors containing the GluR5 subunit (GluR5KRs) regulate GABAergic inhibitory synaptic transmission via both postsynaptic and presynaptic mechanisms. The relevance of these findings to epilepsy is suggested by additional findings that a) activation of GluR5KRs can induce epileptiform activity in in vitro amygdala slices, and epilepsy in vivo, b) expression of these receptors is elevated in epileptic temporal lobe regions, in both humans and rats, c) GluR5-KRs are a primary target of a commonly used antiepileptic drug (topiramate), and d) GluR5-KR antagonists prevent limbic seizures. We are working on identifying the alterations in GABAergic and glutamatergic synaptic transmission, in the BLA, during the course of epileptogenesis, and determining whether changes in the function of GluR5KRs contribute to these alterations. We will also determine whether genetic elimination or pharmacological blockade of GluR5KRs can inhibit epileptogenesis. Unraveling the role of GluR5KRs in the pathogenesis of epilepsy may have significant implications for the discovery of antiepileptogenic drugs that have fewer side effects, as GluR5KR antagonist do not affect normal synaptic transmission and GluR5KRs are not widely distributed in the brain.

In summary, the goal of our research program is to provide the basic knowledge that is necessary for the development of effective therapeutic strategies aimed at preventing or treating certain neurological and psychiatric disorders where dysfunction of the amygdala plays a pivotal, causative role.

Project 1: INCREASING BRAIN ACIDITY MAY REDUCE ANXIETY - Animal study highlights potential new target for treating anxiety disorders

The lifetime prevalence of anxiety disorders (generalized anxiety disorder, panic disorder, social phobia, posttraumatic stress disorder, and obsessive-compulsive disorder) is already more than 20% in the general population, and it is only rising. The associated personal and societal burden is considerable. Available psychotropic drug treatments require careful selection and close patient monitoring, and are often ineffective or have serious adverse effects. Dr. Maria Braga and colleagues (APG USUHS) reported a novel mechanism associated with the generation and expression of anxiety, which may potentially lead to the development of new pharmacological treatments for anxiety disorders (The Journal of Neuroscience, 2014 Feb 26;34(9):3130-41).

This study was performed in Dr. Braga’s lab at USU with the participation of 3 neuroscience graduate students*, and was authored by Pidoplichko VI, Aroniadou-Anderjaska V, Prager EM*, Figueiredo TH, Almeida-Suhett CP*, Miller SL*, and Braga MFM. The Society for Neuroscience covered their paper entitled "ASIC1a Activation Enhances Inhibition in the Basolateral Amygdala and Reduces Anxiety" in a press release. The Press Release was also published in ScienceDaily which is one of the Internet's most popular science news web sites. Since starting in 1995, this award-winning site has earned the loyalty of students, researchers, healthcare professionals, government agencies, educators and the general public around the world. Now with more than 3 million monthly visitors, ScienceDaily generates nearly 15 million page views a month and is steadily growing in its global audience. Please see the press release at https://www.eurekalert.org/pub_releases/2014-02/sfn-iba022414.php or you may also contact Dr. Maria Braga to request a pdf copy of the SFN press release.

Below, please find other articles published by Maria's team elucidating new and important mechanisms regulating neuronal excitability in the amygdala, and the discussion of how alterations in these mechanisms play a critical role in anxiety disorders and epilepsy.

NIH Sponsored Selected Publications:
Pidoplichko VI, Aroniadou-Anderjaska V, Prager EM, Figueiredo TH, Almeida-Suhett CP, Miller SL, Braga MF. ASIC1a activation enhances inhibition in the basolateral amygdala and reduces anxiety. J Neurosci. 2014 Feb 26;34(9):3130-41.

Aroniadou-Anderjaska V, Pidoplichko VI, Figueiredo TH, Braga MFM. Oscillatory Synchronous Inhibition in the Basolateral Amygdala and its Primary Dependence on NR2A-containing NMDA Receptors. Neuroscience. 2018 Mar 1;373:145-158.

Pidoplichko VI, Prager EM, Aroniadou-Anderjaska V, Braga MF. α7-Containing nicotinic acetylcholine receptors on interneurons of the basolateral amygdala and their role in the regulation of the network excitability. J Neurophysiol. 2013 Nov;110(10):2358-69.

Aroniadou-Anderjaska V, Pidoplichko VI, Figueiredo TH, Almeida-Suhett CP, Prager EM, Braga MF. Presynaptic facilitation of glutamate release in the basolateral amygdala: a mechanism for the anxiogenic and seizurogenic function of GluK1 receptors. Neuroscience. 2012 Sep 27;221:157-69.

Williams LR, Aroniadou-Anderjaska V, Qashu F, Finne H, Pidoplichko V, Bannon DI, Braga MF. RDX binds to the GABA(A) receptor-convulsant site and blocks GABA(A) receptor-mediated currents in the amygdala: a mechanism for RDX-induced seizures. Environ Health Perspect. 2011 Mar;119(3):357-63.

PROJECT 2: EBBING GABA SUPPLY EXPLAINS WHY MILD TRAUMATIC BRAIN INJURY EFFECTS SLOW TO SHOW

About three quarters of people who suffer mild traumatic brain injury (mTBI)—such as soldiers who survive explosive device blasts and athletes concussed on the playing field—experience memory loss, lack of concentration, increases in anxiety, and changes in hippocampal function, even where no structural damage can be seen. In a consortium organized and led by Dr. Maria Braga (APG - USUSH) through the multi-institutional Center for Neuroscience and Regenerative Medicine (CNRM), research teams from the NIMH (Lee Eiden, PhD, Chief, Section on Molecular Neuroscience and Zheng Li, PhD, Chief, Section on Synapse Development Plasticity) and the Uniformed Services University of the Health Sciences (USUHS) (Maria F. Braga, DDS, PhD and Ann Marini, PhD, MD) have worked together to refine our understanding of how mTBI affects the brain. Working with rat models, the researchers were able to show that even one incident of mild controlled cortical impact (mCCI) can affect inhibitory interneurons’ ability to biosynthesize GABA. The resultant decrease in GABAergic tone subsequently disrupted synaptic transmission, which in turn increased anxiety. The experimenters further demonstrated that, because the loss of GABAergic function is gradual, the effects are frequently not observed until some time after an mTBI incident. These findings suggest that bolstering GABAergic neuronal function could possibly slow or even reverse deleterious changes that occur following mTBI.

Additionally, the USUHS and NIMH researchers used multi-read miRNA analysis (Dr. Li’s lab) and transcriptome microarray analysis, carried out by NIMH post-bac IRTA Cameron Waites (Pat Tilmon Scholar in residence 2013-2015; now completing medical training at Massachusetts General Hospital, Boston) to show that mCCI is immediately followed by cytokine-associated changes in non-neuronal brain compartments and in neuronal miRNA—changes that may be linked to later effects of mTBI on neuronal transmission. If the consortium receives support to continue its study of TBI, the researchers propose to test precisely how initial insult to the brain is linked neurochemically with the cascade that leads to decreased GABAergic function over a period of days, and to altered emotion and behavior over a period of weeks. Establishing and understanding causal links such as these is a first step toward the development of more effective treatments—and perhaps even to reversing adverse neuronal effects of traumatic brain injury.

This Research Program was described in an article in BrainWaves (2016), the NIMH in-house organ for disseminating information about intramural research, including collaborative research. You may contact Maria Braga to request a pdf copy of the BrainWaves article.

USUHS-NIMH CNRM-Sponsored Publications:
Figueiredo TH, Harbert CL, Pidoplichko V, Almeida-Suhett CP, Pan H, Rossetti K, Braga MFM, Marini AM. Alpha-Linolenic Acid Treatment Reduces the Contusion and Prevents the Development of Anxiety-Like Behavior Induced by a Mild Traumatic Brain Injury in Rats. Mol Neurobiol. 2018 Jan;55 (1):187-200.

Camila P. Almeida-Suhett, Eric M. Prager, Volodymyr Pidoplichko, Taiza H. Figueiredo, Ann M. Marini, Zheng Li, Lee E. Eiden, Maria F. M. Braga. GABAergic Interneuronal Loss and Reduced Inhibitory Synaptic Transmission in the Hippocampal CA1 Region after Mild Traumatic Brain Injury. Experimental Neurology Nov 2015(273):11–23.

Samal BB, Waites CK, Almeida-Suhett C, Li Z, Marini AM, Samal NR, Elkahloun A, Braga MF, Eiden LE. Acute Response of the Hippocampal Transcriptome Following Mild Traumatic Brain Injury After Controlled Cortical Impact in the Rat J Mol Neurosci. Oct 2015 (57)2:282-303.

Almeida-Suhett CP, Prager EM, Pidoplichko V, Figueiredo TH, Marini AM, Li Z, Eiden LE, Braga MF. Reduced GABAergic Inhibition in the Basolateral Amygdala and the Development of Anxiety-like Behaviors after Mild Traumatic Brain Injury. PLoS One. Jul 21, 2014(9)7:e102627.

Camila P. Almeida-Suhett, Zheng Li, Ann M. Marini, Maria F.M. Braga, and Lee E. Eiden.
Temporal Course of Changes in Gene Expression Suggests a Cytokine-Related Mechanism for Long-Term Hippocampal Alteration after Controlled Cortical Impact. J Neurotrauma Apr 1 2014 (31)7:683-690.

Zhonghua Hu, Danni Yu, Camila Almeida-Suhett, Kang Tu, Ann M. Marini, Lee Eiden,
Maria F. Braga, Jun Zhu, Zheng Li. Expression of miRNAs and Their Cooperative Regulation of the Pathophysiology in Traumatic Brain Injury. PLoS One 2012(7)6:e39357.

PROJECT 3: NEW DRUG STRIKES NERVE AGENT

Nerve agents are deadly chemical weapons that are presently a serious threat to military and civilian populations. Nerve agents have been used in the Iraq-Iran war, against Kurdish civilians, in terrorist attacks in Japan, and most recently, the world has witnessed, once again, the devastating effects of nerve agent attacks against civilians in Syria and in England. Currently FDA-approved medical countermeasures are inadequate in counteracting many of the acute intoxication symptoms, including arresting nerve agent-induced seizures (status epilepticus), and preventing brain damage, which leads to long-term neurological and neuropsychiatric disorders. Dr. Maria Braga and colleagues (APG USUHS) has discovered that Tezampanel (also known as LY- 293,558), an antagonist of the GluK1 Kainate Receptors and AMPA receptors, is very effective against nerve agent-induced seizures and neuropathology. Maria Braga conceived the initial idea in 2006, and obtained support from the National Institute of Neurological Disorders and Stroke (NINDS) to demonstrate the proof-of-concept. Since then, and with continuous support from NINDS, Maria and her team have conducted extensive pre-clinical studies demonstrating the effectiveness of Tezampanel against these weapons of mass destruction, even when the drug was administered with a significant delay after exposure to a nerve agent. Encouraged by the very promising results of her investigations, Maria convinced Eli Lilly to form a new company (Proniras) to further develop Tezampanel. On Friday, April 25, 2018, it was announced that the Biomedical Advanced Research and Development Authority (BARDA) has awarded a $89.5 million contract to Proniras for the advanced research development of Tezampanel (also known as LY- 293,558), for the treatment of nerve agent induced-seizures that are refractory to benzodiazepines. These further studies are likely to result in the development of a novel, safe and effective therapeutic treatment against nerve agent-induced seizures and brain damage that will enhance our treatment response capabilities during an emergency.

This Research Program was described in an article in DVIDS – Defense Visual Information Distribution Service (2018). DVIDS is a state-of-the-art, 24/7 operation owned by DMA (Defense Media Activity) that provides a timely, accurate and reliable connection between the media around the world and the military serving at home and abroad. Please see the press release at https://www.dvidshub.net/news/289618/new-drug-strikes-nerve-agent or you may contact Maria Braga to request a pdf copy of the DVIDS article.

NIH/DTRA Sponsored Selected Publications:
Figueiredo TH, Apland JP, Braga MFM, Marini AM. Acute and long-term consequences of exposure to organophosphate nerve agents in humans. Epilepsia. 2018 Oct;59 Suppl 2:92-99.

Apland JP, Aroniadou-Anderjaska V, Figueiredo TH, Pidoplichko VI, Rossetti K, Braga MFM. Comparing the Antiseizure and Neuroprotective Efficacy of LY293558, Diazepam, Caramiphen, and LY293558-Caramiphen Combination against Soman in a Rat Model Relevant to the Pediatric Population. J Pharmacol Exp Ther. 2018 May;365(2):314-326

Aroniadou-Anderjaska V, Figueiredo TH, Apland JP, Prager EM, Pidoplichko VI, Miller SL, Braga MF. Long-term neuropathological and behavioral impairments after exposure to nerve agents. Ann N Y Acad Sci. 2016 Jun;1374(1):17-28.

Prager EM, Aroniadou-Anderjaska V, Almeida-Suhett CP, Figueiredo TH, Apland JP, Rossetti F, Olsen CH, Braga MF. The recovery of acetylcholinesterase activity and the progression of neuropathological and pathophysiological alterations in the rat basolateral amygdala after soman-induced status epilepticus: relation to anxiety-like behavior. Neuropharmacology. 2014 Jun;81:64-74.

Prager EM, Figueiredo TH, Long RP 2nd, Aroniadou-Anderjaska V, Apland JP, Braga MF. LY293558 prevents soman-induced pathophysiological alterations in the basolateral amygdala and the development of anxiety. Neuropharmacology. 2015 Feb;89:11-8.

Prager EM, Pidoplichko VI, Aroniadou-Anderjaska V, Apland JP, Braga MF. Pathophysiological mechanisms underlying increased anxiety after soman exposure: reduced GABAergic inhibition in the basolateral amygdala. Neurotoxicology. 2014 Sep;44:335-43

Figueiredo TH, Aroniadou-Anderjaska V, Qashu F, Apland JP, Pidoplichko V, Stevens D, Ferrara TM, Braga MF. Neuroprotective efficacy of caramiphen against soman and mechanisms of its action. British Journal of Pharmacology 2011 Nov;164(5):1495-505.

1963 B.A. (Physics, Math minor), San Diego State College, San Diego, California
1965 M.S. (Physics), San Diego State College, San Diego, California
1973 Ph.D. (Physics), University of Arizona, Tucson, Arizona

PhD (Pharmacology) - University of Pennsylvania, Philadelphia, PA, 2005
MA (Chemistry) - Temple University, Philadelphia, PA, 2000
BS (Chemistry) - Temple University, Philadelphia, PA, 1998

The primary research goal of the lab is to identify the genetic causes and clarify the molecular mechanisms underlying neurodegenerative diseases. Using a combination of cell and molecular biology approaches we investigate how changes to cellular protein homeostasis impact human diseases.

Current research projects include (i) elucidating the signaling cascade that modulate the stability of the survival motor neuron (SMN) protein, which is deficient in spinal muscular atrophy (SMA), (ii) investigating the role of proteasome dynamics in traumatic brain injury, (iii) identifying small molecule therapeutics to treat neurological disorders using mouse models and (iv) identifying new genes associated with hereditary neurological disorders. These projects are designed to reveal novel clinical entities and therapeutic targets for treating disorders of the nervous system.

Postdoctoral Fellowship 2004-2007 Georgetown University
Postdoctoral Fellowship 2003-2004 Uniformed Services University
PhD 2003 Uniformed Services University
BS 1997 University of Pittsburgh

Ph.D. in Pharmacology, St. Mary's Hospital Medical School, University of London, London, United Kingdom, 1965
B.Sc. in Pharmacolopy, Chelsea College of Science & Technology, University of London, London, United Kingdom, 1962

Dr. Cox is currently Professor of Pharmacology and Neuroscience at the Uniformed Services University (USU) in Bethesda MD. He received his initial training in pharmacology from Chelsea College of Science and Technology in London, UK, and received a Ph.D. in Pharmacology from St. Mary's Hospital Medical School, University of London, UK. After teaching pharmacology to pharmacy and science students at Chelsea College of Science and Technology of the University of London for eight years, he became a visiting scientist in the Department of Pharmacology at Stanford University, and was appointed Consulting Associate Professor of Pharmacology at Stanford in 1978. Concurrently, he served as Laboratory Research Group Director and then Associate Director for Research for the Addiction Research Foundation in Palo Alto, CA. In 1981, Dr. Cox moved to his current position at USU, where he served as chair of the Department of Pharmacology from 1995 until 2007. He currently also serves as an Assistant Dean for Graduate Education at USU.
For most of his career Dr. Cox's research has focused on characterizing the receptors utilized by opiate drugs and their endogenous ligands, and in defining potential physiological and pathophysiological roles for endogenous opioids and other neuropeptides. His lab is currently studying factors affecting peptide and receptor expression, and changes at the cellular level induced by drugs of abuse, severe stress, or neural injury. He now leads the Biomarkers Group of the USU/NIH Center for Neuroscience and Regenerative Medicine, evaluating neurochemical mechanisms underlying traumatic brain injury and potential biomarkers for TBI.
Dr. Cox has been a member of the American Society for Pharmacology and Experimental Therapeutics (ASPET) since 1976. He served as Secretary/Treasurer of (1997-2000), and was elected President of ASPET for 2009-2010. He chaired the ASPET Board of Publications Trustees from 2002-2007. He has served on the Editorial Boards of the Journal of Pharmacology and Experimental Therapeutics (1998 – present), Molecular Pharmacology (1981-1994), and Molecular Interventions (2000-2002). Dr. Cox was a member of the ASPET Scientific Program Committee from 1986-1990 and Chaired the Program Committee from 1990-1996. He served as ASPET’s representative to the Experimental Biology Program Committee from 1991-1994 and served on the Experimental Biology Board from 1996-1999 (as Chairman for 1998-1999). He is currently serving a second term as a member of the Board of Directors of the Federation of American Societies of Experimental Biology.

Dr. Cox was the ASPET representative to the International Advisory Committee for the 1998 International Union of Pharmacology (IUPHAR) Congress in Munich, Germany, and chaired the IUPHAR World Congress of Pharmacology Scientific Program Committee for the 2002 meeting, held in San Francisco, CA. He is also a member of the British Pharmacological Society, the Society for Neuroscience, the AAAS, the American Society for Neurochemistry, and the International Narcotics Research Conference (for which he served as President from 1994-1998).

College of William and Mary A.B. 01/1971 Mathematics
College of William and Mary M.A. 05/1978 Physical Ed/Education
University of Maryland Ph.D. 051982 Nutr Sci & Biochem
USUHS School of Medicine Post-Doc 07/1982 Physiology
USUHS School of Medicine M.P.H. 12/1995 Epidemiology

Patricia A. Deuster, PhD, MPH, is a Professor in the Department of Military and Emergency Medicine at the Uniformed Services University of the Health Sciences (USU) in Bethesda, Maryland and Director for the Consortium for Health and Military Performance (CHAMP), the Defense Center of Excellence for Human Performance Optimization Translation. She obtained an AB in Mathematics and Computer Science and MA in Education and Physical Education from the College of William and Mary, a PhD in Nutritional Sciences and Physiology from the University of Maryland, and a MPH with an emphasis in public health and epidemiology from USU.

Dr. Deuster chairs the Department of Defense (DoD) Dietary Supplement Subcommittee, is a member of the DoD Food and Nutrition Subcommittee, serves on the DoD Human Performance Optimization Committee, the VA/DoD Health Executive Committee Women's Health Work Group, the DoD Nutrition Committee, and the DoD Population Health Working Group. She is a Fellow of the American College of Sports Medicine, a Certified Nutrition Specialist, and has over 200 peer-reviewed papers and numerous book chapters and books relating to human performance with a focus on health, total force fitness, nutrition, dietary supplements, physical performance, and exertional-related health events. In addition she has developed multiple educational materials related to human performance and total force fitness: Visit the CHAMP Human Performance Resource Center (hprc-online.org) and Operation Supplement Safety (OPSS.org) websites. Dr. Deuster is a member of the Order of Military Medical Merit and received the Special Operations Medical Researcher Award from the Special Operations Medical Association in 2014.

1995 Ph.D. in Pysiology, University College London, United Kingdom
1990 BSc with honours in Biological Sciences, Birmingham, United Kingdom

My research interest is in neurogenesis with a particular focus on the transcriptional control of neuronal specification and differentiation. My early training investigated cerebellar development in spontaneous mutant mice models using classical histochemistry and electron microscopy techniques. As a postdoctoral researcher and later a Research Assistant Professor, I gained considerable experience in the creation and application of transgenic and targeted mutant mouse models in neurodevelopment research at The Rockefeller University. More recently my work has focused on using human induced pluripotent stem cells to model physiological and pathophysiological mechanisms of neuronal network connectivity in vitro. I am particularly interested in the role epigenetic factors play in neurogenesis and I have published several peer-reviewed publications on this topic in the last few years.

University of Wroclaw, Department of Experimental Physics, Wroclaw, Poland. M.Sc.
Academy of Medicine, Wroclaw, Poland, Ph.D.
Laboratory of Neurosciences, NIA, NIH, Postdoctoral

1986-1988 Visiting Fellow, research in electrophysiology and teaching- lecturer graduate students Course on Cellular Biophysics and Physiology, Biophysics Laboratory, International School for Advanced Studies (SISSA), Trieste, Italy.
1987 Research Fellow, postdoctoral studies in electrophysiology under supervision of Dr. Franco Conti, Institute of Cybernetics and Biophysics, CNR, Genova- Camogli, Italy.
1990-1994 Visiting Associate, Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD.
1994-1999 Chief, Unit on Cell Pathophysiology, Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD.
2000-2004 Assistant Professor Department of Anatomy, Physiology and Genetics, USUHS, School of Medicine, Bethesda MD.
2004-2012 Associate Professor Department of Anatomy, Physiology and Genetics, USUHS, School of Medicine, Bethesda MD.
2012-present Professor, Department of Anatomy, Physiology and Genetics (Primary appointment), Neuroscience and Molecular and Cell Biology Program (Secondary appointments), USUHS, School of Medicine, Bethesda MD.

B.S., Medical Microbiology, Stanford University (1975)
M.A. (1977), M.Phil. (1979), and Ph.D. (1980) degrees in Physiological and Social Psychology, Columbia University
Doctoral training in Pharmacology, Columbia University’s College of Physicians & Surgeons under a National Research Service Award (1976-79).

Neil E. Grunberg, Ph.D., is Professor of Military & Emergency Medicine (MEM), Medical & Clinical Psychology (MPS), and Neuroscience (NES) in the Uniformed Services University (USU) School of Medicine (SOM); Professor in the Graduate School of Nursing (GSN); Director of Research and Development in the USU Leadership Education and Development (LEAD) program; and Director of Faculty Development for MEM. He is a medical and social psychologist who has been on faculty at USU since 1979. His role in LEAD is to ensure that the LEAD program and sessions are based upon sound evidence and scholarship and to oversee research relevant to leadership education and training (see www.usuhs.edu/usulead).

Dr. Grunberg earned baccalaureate degrees in Medical Microbiology and Psychology from Stanford University (1975); earned M.A. (1977), M.Phil. (1979), and Ph.D. (1980) degrees in Physiological and Social Psychology from Columbia University; and received doctoral training in Pharmacology at Columbia University’s College of Physicians & Surgeons under a National Research Service Award (NRSA, 1976-79). Dr. Grunberg helps train physicians, psychologists, and nurses to serve in the Armed Forces or Public Health Service, and scientists for research positions. He has published >180 papers addressing behavioral medicine, stress, and leadership. Dr. Grunberg has received awards from the U.S. Surgeon General, CDC, FDA, American Psychological Association, NIH, Society of Behavioral Medicine, and USU. He has served as President of the USU Faculty Senate and has chaired USU committees including: Strategic Planning; Manpower; Health, Safety, and Wellness; Appointment, Promotions, and Tenure. Outside USU, he has chaired Working Groups for the MacArthur Foundation and Robert Wood Johnson Foundation. In 2015, Dr. Grunberg was selected as a Presidential Leadership Scholar (PLS).

Dr. Grunberg and his research group (see www.usuhs.edu/faculty/grunberg) study leadership, stress (psychological and physical, including mTBI and PTSD), and appetitive behaviors (including nicotine, alcohol, caffeine, and food consumption). His teaching includes topics in leadership, social psychology, psychobiology, behavioral neuroscience, and sports psychology.

Dr. Grunberg has supervised 35 doctoral dissertations in Medical Psychology, Clinical Psychology, and Neuroscience, and has served on many master and doctoral degree committees. He currently is training a Clinical Psychology Ph.D. student and a GSN Ph.D. student. In addition, he mentors faculty members in MEM in his role as MEM Director of Faculty Development.

Bachelor of Arts - Temple University
Occupational Therapy Advanced Degree - U of Pennsylvania
Doctor of Philosophy - U of Pennsylvania

I completed my Ph.D. requirements in the Department of Biochemistry, Georgetown University School of Medicine and Dentistry the summer prior to matriculating into medical school at the same institution. My Ph.D. degree was conferred on me two years prior to graduating from medical school at Georgetown University School of Medicine and Dentistry. During my clinical rotations as a medical student, I became very interested in Internal Medicine and mentors at Georgetown University encouraged me to pursue this field because it would provide me with the fundamentals I would need should I decide to further advance my career. To this end, I completed an Internal Medicine Residency at the University of Massachusetts, Worcester, Massachusetts. During the second year of my medicine residency, I became interested in the field of Neurology due in part to the excellent faculty in the Neurology Department at the University of Massachusetts chaired by David Drachman, M.D. During this time, I participated in a small project to understand the underlying mechanism(s) of valproic acid-induced hyperammonemia. Along with my co-workers, we published three peer-review papers and demonstrated that valproic acid inhibited carbamyl phosphate I synthase activity in the absence of hepatic dysfunction. My experience with the Neurology faculty and my contribution to three scientific publications on vaproic-induced hyperammonemia propelled me to apply for Neurology residencies. I was accepted into the Albert Einstein College of Medicine program where I completed my Neurology residency. I am board certified in Internal Medicine and Neurology. I wanted to pursue my goal to qualify for an academic position at a medical school so I wrote to the Scientific Director of the National Institute of Neurological Disorders and Stroke (NINDS), Dr. Irwin Kopin, and he hired me as a Senior Staff Fellow. While at NINDS, I developed my skills in Neuroscience research by collaborating with Sanford Markey, Ph.D., in the National Institute of Mental Health (NIMH), on the mechanism of 1-methyl-4-phenylpyridinium (MPP+)-induced parkinsonism. Dr. Markey consulted with Neurology on a very young man who developed parkinsonian signs that responded to anti-parkinsonian drugs. Dr. Markey carefully removed a small amount of a white powder from the young man’s dessicator jar and determined the structure. Dr. Markey provided me with the compound and our group developed a neuronal culture model of MPP+-induced neuronal cell death. Together with my co-workers, our group first demonstrated that MPP+ killed neurons by an apoptotic-mediated mechanism. We also showed in a co-culture of neurons and astrocytes that the addition of the precursor, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), killed the neurons but the astrocytes in the culture remained viable. We later showed that addition of MPTP to a highly purified culture of astrocytes converted MPTP to MPP+ confirming the in vivo results. After leaving Dr. Kopin’s laboratory, I remained a Senior Staff Fellow and was employed by Dr. Steven Paul, Scientific Director of NIMH. It was in his laboratory that we made our most significant discovery. We showed that low-level activation of N-methyl-D-aspartate (NMDA) receptors protected vulnerable neurons against an excitotoxic concentration of glutamate acting on NMDA receptors. This was the first time that NMDA receptors were shown to exhibit neuroplastic effects. We demonstrated that the underlying mechanism was the immediate release of brain-derived neurotrophic factor (BDNF) that in turn bound to and activated TrkB receptors in an autocrine fashion followed by the later synthesis and release of BDNF. BDNF was required for the NMDA receptor-mediated neuroprotective effect. The discovery of the neuroplastic effects mediated by NMDA receptors on neurons provided the fundamental building blocks of my current research. Along with my colleagues, I was first to demonstrate that administration of the nutraceutical α-linolenic acid (LIN) at 30 min, 3 days and 7 days after soman exposure by intravenous injection significantly reduced soman-induced neuropathology in adult male rats that lasts up to three weeks after soman exposure, long after the last LIN injection suggesting that the nutraceutical LIN exerts secondary effects. LIN significantly increased animal survival. Exposure to soman resulted in profound behavior deficits in rodents. Our group demonstrated that administration of LIN at 30 min, 3 days and 7 days after soman exposure significantly increased the amount of time the animals spent on the rotarod, reversed the depressive-like behavior of the soman-exposed animals and significantly improved memory retention in the passive avoidance task. The anti-depressant effect in those animals that were administered LIN after soman exposure was associated with a significant increase of the major neuroprotective protein mature BDNF in the hippocampus, a protein with well-established anti-depressive effects. We also showed that administration of LIN at 30 min, 3 days and 7 days after soman exposure significantly increased the number of immature and later mature neurons in the subgranular zone of the dentate gyrus over baseline. We further showed that the activated form of the mammalian target of rapamycin complex 1 (mTORC1) and activated Akt were only increased in the hippocampus from animals that were administered with LIN at 30 min, 3 days and 7 days after soman exposure. Rapamycin, a well-established blocker of mTORC1, was used to determine the role of this serine/threonine kinase in the LIN-induced neurogenesis. The significant deficit induced by soman in the passive avoidance task and the requirement of the amygdala and hippocampus for the successful performance of this test provided a unique opportunity to evaluate the magnitude of LIN to restore cognitive function. The ability of LIN to improve performance was expected to be difficult because the most damage occurs in these two brain regions after soman exposure. We confirmed that the intravenous administration of LIN at 30 min, 3 days and 7 days after soman exposure resulted in a significant improvement in retention latency of the passive avoidance task in soman-exposed animals. Administration of rapamycin, however, completely blocked the LIN-induced improvement in retention latency and the LIN-induced increase in neurogenesis suggesting that enhanced neurogenesis induced by LIN plays a critical role in the LIN-induced improvement in retention latency in the passive avoidance via an mTORC1-mediated mechanism. The downstream mTORC1 pathway is likely activated by the increase in activated Akt via a BDNF-TrkB-mediated mechanism. Taken together, the nutraceutical LIN exhibits pleotropic properties in the brain that significantly reduces soman-induced neuropathology, strikingly increases neurogenesis in the subgranular zone of the dentate gyrus and significantly improves performance on standard behavioral tasks. The overarching goal of my research in the Department of Neurology and Program in Neuroscience at the Uniformed Services University of the Health Sciences is to discover and delineate endogenous neuroprotective pathways in brain as well as discover nutraceuticals and drugs with minimal side effects that upregulate these endogenous survival pathways in brain to protect against neurodegenerative disorders.

School Degree Dates

Rutgers College Bachelor of Arts June 1974
New Brunswick, New Jersey

University of Wisconsin Master of Science in December 1976
Oshkosh, Wisconsin Clinical Psychology

City University of New York Master of Philosophy July 1983
New York, New York Doctor of Philosophy in
Neuropsychology

Dr. Joseph McCabe is Professor and Vice Chair for Faculty Affairs of the Department of Anatomy, Physiology and Genetics, and a Professor in the Neuroscience and the Cell and Molecular Biology Graduate Programs at USU. He received his undergraduate training in psychology and biology at Rutgers College, an M.S. degree in clinical psychology from the University of Wisconsin-Oshkosh, and M.Phil. and Ph.D. degrees from the City University of New York. Dr. McCabe spent 11 years at The Rockefeller University before his move to USU. He serves as the Program Director for Neuroprotection and Modeling of The Center for Neuroscience and Regenerative Medicine. His laboratory is interested in understanding the mechanisms of cell response to stress and in the development of pharmacological therapies that may reduce the functional consequences of brain injury.

INSTITUTION AND LOCATION DEGREE YEAR(s) FIELD OF STUDY
Rice University, Houston, TX B.A. 1964 Biology
University of Chicago, Chicago, IL M.D. 1969 Medicine
University of Chicago, Chicago, IL Ph.D. 1973 Biochemistry

Dr. Pollard received his undergraduate degree from Rice University, and his MD and PhD (in Biochemistry) degrees from the University of Chicago. Following postdoctoral training at the NIH and at Oxford University, Dr. Pollard returned to the NIH in the U.S. Public Health Service (USPHS), eventually becoming intramural Chief of the Laboratory of Pathology, and then Chief of the Laboratory of Cell Biology and Genetics, NIDDK. Dr. Pollard subsequently moved across Wisconsin Avenue to become Chair of the Department of Anatomy, Physiology and Genetics, in the Uniformed Services University School of Medicine, Bethesda, MD. Dr. Pollard’s principal hypothesis-driven research focus has been on proinflammatory mechanisms. Dr. Pollard is the Founding Director of the Collaborative Health Initiative Research Program (CHIRP), a whole genome sequencing (WGS) program of investigation, jointly sponsored by NHLBI and the Department of Defense. In addition, Dr. Pollard is also Founding Director of The American Genome Center (TAGC), a Department of Defense entity that is one of only four academic Genome Centers in the United States.The goals of CHIRP and the TAGC are to develop “precision medicine” as an aid to diagnosis and treatment of disorders of common interest in both civilian and military disease cohorts. Dr. Pollard has received the NIH Inventor’s Award, and has authored nearly 350 peer reviewed scientific publications and numerous invited chapters.

B.S., Animal Sciences (1999), University of Massachusetts, Amherst
Ph.D., Molecular and Cellular Biology and Animal Sciences (2004), University of Massachusetts, Amherst
Post-doctoral Training, National Institute of Environmental Health Sciences, National Institutes of Health

B.Sc.(Hons). Biochemistry, University of Manchester, UK
Ph.D. Biochemistry/Molecular Biology, University College London, UK
Post-doctoral training: Massachusetts General Hospital/ Harvard Medical School, Boston.

RESEARCH INTERESTS:

My lab aims to understand the mechanisms through which the brain responds to traumatic injury and more specifically to delineate the pathways through which detrimental neuroinflammatory cascades can be altered to enhance recovery after injury. The initial lesion can produce significant tissue damage and breakdown of the blood brain barrier. These immediate effects lead to activation of many secondary cascades involving interplay between endogenous surviving neurons and glia, and infiltrating cells and molecules from the bloodstream. Injury therefore leads to acute neuroinflammatory cascades, and also to more chronic inflammatory effects. Indeed, activated microglia have been documented in postmortem brains many years after the initial insult. Our lab focuses on understanding the molecular signaling cascades that occur after injury in addition to testing potential therapeutics to enhance recovery from injury. We currently utilize several different rodent models of traumatic brain injury (TBI), with assays ranging from behavioral through molecular to understand the complex interactions that occur after injury, and to determine how manipulations may impact on functional recovery. We also utilize primary cell cultures to tease apart the molecular signaling pathways that contribute to inflammation after injury.

Angiotensin receptor blockers as potential therapeutics for TBI
Angiotensin receptor blockers (ARBs) are widely used FDA-approved anti-hypertension drugs with a favorable side effect profile that have been used as a mechanism for reducing the amount of TGF-β signaling in several different organ systems. In the CNS, ARBs have also been shown to be neuroprotective, anti-inflammatory and protective of the cerebral blood flow (CBF). The brain possesses its own renin angiotensin system, with many different components of the system expressed in the different cell types in the brain. However, in addition to acting as antagonists at the Angiotensin II receptor 1 (AT1R) some ARBs also possess potent PPARγ agonist activity that enhances their anti-inflammatory action. We have demonstrated that the ARB candesartan, lessens inflammation, reduces lesion volume, limits glial reactivity, increases neuronal survival and improves motor and cognitive recovery up to 28 days after injury. These beneficial effects are seen when low-dose candesartan is administered up to 6 hours after injury, a clinically acceptable therapeutic window. Our data suggest that both AT1 receptor antagonism and PPARγ agonism contribute to the efficacy of ARB treatment after TBI and it is this multimodal action by a single drug that makes it a strong candidate for TBI clinical trials. We are pursuing translational studies for candesartan for brain injury in addition to investigating the consequences of TBI on the endogenous renin-angiotensin system in the brain.

TGF-β signaling after injury
TGF-β is an injury induced cytokine that has complex roles in the central nervous system. After brain injury TGF-β can promote astrogliosis and enhance the deposition of molecules inhibitory to regeneration in the glial scar. Yet TGF-β is also neuroprotective indicating the sometimes conflicting roles of this cytokine. We have shown that after a penetrating brain injury mice that lack expression of the TGF-β signaling molecule Smad3, form a glial scar more quickly, with a smaller scar, than wild type mice. However, we also found that Smad3 null mice have more pronounced neuronal loss after injury. Thus, global interference with TGF-β signaling is not a desirable therapeutic option. Further, TGF-β is anti-inflammatory in some contexts – so chronic repression of TGF-β signaling pathways may enhance inflammation. In primary microglial cultures we have shown that inflammatory pathways downregulate TGF-β receptor expression, allowing for prolonged enhancement of the inflammatory activated state.

B.S., Magna Cum Laude, University of Notre Dame, 1969
M.D., Yale University, 1973
Psychiatry Resident, Wilford Hall USAF Medical Center, 1973-75
Postdoctoral Fellow (Psychiatry) Yale University & Yale
USAF Primary Course in Aerospace Medicine, Brooks Air Force Base Texas, 1977
Washington Psychoanalytic Institute, 1980-1986 (graduated)

Dr. Ursano is Professor of Psychiatry and Neuroscience at the Uniformed Services University, Bethesda, Maryland. He is founding Director of the Center for the Study of Traumatic Stress and served as the Chairman of the Department of Psychiatry at USU for 25 years (1992-2017). In addition, Dr. Ursano is Editor of Psychiatry, the distinguished journal of interpersonal and biological processes, founded by Harry Stack Sullivan. Dr. Ursano completed twenty years of service in USAF medical corps and retired as Colonel in 1991. He was educated at the University of Notre Dame and Yale University School of Medicine and did his psychiatric training at Wilford Hall USAF Medical Center and Yale University.

Dr. Ursano served as the Department of Defense representative to the National Advisory Mental Health Council of the National Institute of Mental Health and is a past member of the Veterans Affairs Mental Health Study Section and the National Institute of Mental Health Rapid Trauma and Disaster Grant Review Section. He is a Distinguished Life Fellow in the American Psychiatric Association. He is a Fellow of the American College of Psychiatrists.Dr. Ursano was the first Chairman of the American Psychiatric Association’s Committee on Psychiatric Dimensions of Disaster. This work greatly aided the integration of psychiatry and public health in times of disaster and terrorism. Dr. Ursano was an invited participant to the White House Mental Health Conference in 1999. He has received the Department of Defense Humanitarian Service Award and the highest award of the International Traumatic Stress Society, The Lifetime Achievement Award, for “outstanding and fundamental contributions to understanding traumatic stress.” He is the recipient of the William C. Porter Award from the Association of Military Surgeons of the United States, and a frequent advisor on issues surrounding psychological response to trauma to the highest levels of the US Government and specifically to the Department of Defense leadership.

Dr. Ursano has served as a member of the National Academies of Science, Institute of Medicine, Committee on Psychological Responses to Terrorism, Committee on PTSD and Compensation and the Committee on Nuclear Preparedness; and the National Institute of Mental Health Task Force on Mental Health Surveillance After Terrorist Attack. In addition he is a member of scientific advisory boards to the Secretary of Health and Human Services and the Centers for Disease Control. In 2012, Dr. Ursano was awarded the William C. Menninger Memorial Award for distinguished contributions to the Science of Mental Health by the American College of Physicians. In 2014, Dr. Ursano and Dr. Matthew Friedman of the VA National Center for PTSD co-founded The Leahy-Friedman National PTSD Brain Banksupported through Senator Patrick Leahy (D-VT). It is the first human brain bank dedicated to PTSD. This joint effort of many people was a 12 year project developing concepts, pilot data and support. Dr. Ursano has more than 300 publications. He is co-author or editor of eight books.

Professional Honors and Recognition
2016 Joseph Tupin Visiting Professor and Invited Lectureship, University of California, Davis
2015 Pellegrino Lectureship, Eastern Virginia Medical University
2014 Uniformed Services University James J. Leonard Award for Excellence in Research
2012 American College of Physicians: William C Menninger Memorial Award for Distinguished Contributions to Mental Health
2008-11 Appointed Mental Health Advisory Subcommittee, National Bioterrorism Science Advisory Board, to Secretary of Health and Human Services
2008-11 Appointed Board of Scientific Counselors, Coordinating Office for Terrorism Preparedness and Emergency Response (name changed to Office of Public Health Readiness), CDC, Department of Health and Human Services
2009 AAP Presidential Citation for Contributions to Psychiatric Education, Association of Academic Psychiatry


Representative Biography of over 400 publications
1. Disaster Medicine. Since its inception in 1987, the Center for the Study of Traumatic Stress (CSTS) has developed research, training, and consultation programs to mitigate the impact of trauma from exposure to war, disasters, terrorism, community violence, and public health threats. The CSTS has helped to define and advance the integration of disaster psychiatry and military psychiatry. CSTS has been involved in nearly every major disaster our nation has experienced in the past nearly 30 years.
a) Ursano, R. J., Fullerton, C. S., Weisaeth, L., & Raphael, B. (Eds.). (2017). Textbook of Disaster Psychiatry (2nd Ed.). Cambridge, England: Cambridge University Press. doi: 10.1017/9781316481424
b) Fullerton, C. S., Mash, H. B. H., Benevides, K. N., Morganstein, J. C., & Ursano, R. J. (2015). Distress of routine activities and perceived safety associated with post-traumatic stress, depression, and alcohol use: 2002 Washington, D.C, Sniper Attacks. Disaster Medicine and Public Health Preparedness, 9(5), 509-515. doi: 10.1017/dmp.2015.67
c) Fullerton, C. S., McKibben, J. B. A., Reissman, D. B., Scharf, T., Kowalski-Trakofler, K. M., Shultz, J. M., & Ursano, R. J. (2013). Posttraumatic stress disorder, depression, alcohol and tobacco use in public health workers following the 2004 Florida hurricanes. Disaster Medicine and Public Health Preparedness, 7(1), 89-95. doi: 10.1017/dmp.2013.6
d) Grieger, T. A., Fullerton, C. S., & Ursano, R. J. (2003). Posttraumatic stress disorder, depression, alcohol use, and perceived safety thirteen months following the terrorist attack on the Pentagon. Psychiatric Services, 54(10), 1380-1383.
2. Risk and protective factors for psychological and behavioral outcomes following traumatic events. Studies examining military and civilian populations exposed to traumatic events has led to research that seeks to identify risk factors for adverse psychological and behavioral outcomes, including posttraumatic stress and depressive symptoms, problematic alcohol use, and suicidal behaviors, as well as protective factors that promote resilience following trauma exposure.
a) Ursano, R. J., Kessler, R. C., Naifeh, J. A., Herberman Mash, H., Fullerton, C. S., Bliese, P. D., Zaslavsky, A. M., Ng, T. H. H., Aliaga, P. A., Wynn, G. H., Dinh, H. M., McCarroll, J. E., Sampson, N. A., Kao, T. C., Schoenbaum, M., Heeringa, S. G., & Stein, M. B. (2017). Risk of suicide attempt among Soldiers in Army units with a history of suicide attempts. JAMA Psychiatry. doi: 10.1001/jamapsychiatry.2017.1925
b) Ursano, R. J., Kessler, R. C., Stein, M. B., Naifeh, J. A., Aliago P. A., Fullerton, C. S., Wynn, G. H., Vegella P. L., Ng, T., Zhang, B. G., Wryter, C. L., Sampson N. A., Kao, T. C., Colpe, L. J., Schoenbaum, M., McCarroll J. E., Cox, K. L., & Heeringa, S., & on behalf of the Army STARRS collaborators (2016). Deployment, mental health, and suicide attempts among U.S. Army soldiers: Risk factors, methods, and time, JAMA Psychiatry, 73(7), 741-749. doi: 10.1001/jamapsychiatry.2016.0600
c) Fink, D. S., Lowe, S., Cohen, G. H., Sampson, L. A., Ursano, R. J., Gifford, R. K., Fullerton, C. S., & Galea, S. (2016). Trajectories of posttraumatic stress symptoms after civilian or deployment traumatic event experiences. Psychological Trauma: Theory, Research, Practice and Policy, 9(2), 138-146. doi: 10.1037/tra0000147
d) Campbell-Sills, L, Ursano, R. J., Kessler, R. C., Sun, X., Heeringa, S. G., Nock, M. K., Sampson, N.A., Jain, S., and Stein, M.B. (in press). Prospective risk factors for post-deployment heavy drinking and alcohol or substance use disorder among U.S. Army soldiers. Psychological Medicine.

3. Identifying biomarkers for posttraumatic stress disorder. Our study of the neuroscience and neurobiology of stress and trauma has translated into health care applications for military and civilian populations, with a specific focus on posttraumatic stress disorder, mild traumatic brain injury, and suicide and suicide-related behaviors. Recent research has focused on genetic biomarkers, cortisol levels, and telomere length. Biomarker research has involved the purification of DNA from saliva samples and blood samples collected from Soldiers, and genotyping the DNA for several target genes including BDNF and FKBP5.
a) Stein, M. B., Chen, C.-Y., Ursano, R. J., Cai, T., Gelernter, J., Heeringa, S. G., Jain, S., Jensen, K. P., Maihofer, A. X., Mitchell, C., Nievergelt, C. M., Nock, M. K., Neale, B. M., Polimanti, R., Ripke, S., Sun, X., Thomas, M. L., Wang, Q., Ware, E. B., Borja, S., Kessler, R. C., & Smoller, J. W. (2016). Genome-wide Association Studies of posttraumatic stress disorder in 2 cohorts of U.S. Army Soldiers. JAMA Psychiatry, 73(7), 695-704. doi: 10.1001/jamapsychiatry.2016.0350.
b) Zhang, L., Hu, X. Z., Benedek, D. M., Fullerton, C. S., Forsten, R. D., Naifeh, J. A., Li, X., Li, H., Benevides, K. N., Smerin, S., Le, T., Choi, K., & Ursano, R. J. (2014). The interaction between stressful life events and leukocyte telomere length is associated with PTSD. Molecular Psychiatry, 19(8), 855-856. doi: 10.1038/mp.2013.14
c) Choi, K., Le, T., Xing, G., Johnson, L. R., & Ursano, R. J. (2011). Analysis of kinase gene expression in the frontal cortex of suicide victims: Implications of fear and stress. Frontiers in Behavioral Neuroscience, 5, 46. doi: 10.3389/fnbeh.2011.00046
d) Zhang, L., Su, T. P., Choi, K., Webster, M., Li, C. T., Chung, M. Y., Chen, Y. S., Bai, Y., Chou, Y., Barker, J., Barrett, J. E., Li, X., H., Benedek, D. M., & Ursano, R. J. (2011). P11 (S100A10) as a potential biomarker of psychiatric patients at risk of suicide. Journal of Psychiatric Research, 45(4), 435-441. doi: 10.1016/j.jpsychires.2010.08.01

4. Translating empirical findings to recommendations for intervention. CSTS laboratory and clinical research actively identifies effective interventions for trauma and stress-related disorders and suicidal behaviors.
a) Ursano, R. J., Goldenberg, M., Zhang, L., Carlton, J., Fullerton, C. S., Li, H., Johnson, L., & Benedek, D. M. (2010). Posttraumatic stress disorder and traumatic stress: From bench to bedside, from war to disaster. Annals of the New York Academy of Sciences, 1208, 72-81. doi: 10.1111/j.1749-6632.2010.05721.x
b) Forbes, D., Creamer, M., Bisson, J., Cohen, J., Crow, B., Foa, E., Friedman, M., Keane, T., Kudler, H., & Ursano, R. J. (2010). A guide to guidelines for the treatment of PTSD and related conditions. Journal of Traumatic Stress, 23(5), 537-562. doi: 10.1002/jts.20565
c) Benedek, D. M. & Ursano, R. J. (2009). Understanding PTSD: From phenomenology to clinical practice. Focus, 7(2), 160-175.
d) Ursano, R. J., Zhang, L., Li, H., Johnson, L., Carlton, J., Fullerton, C. S. & Benedek, D. M. (2009). PTSD and traumatic stress from gene to community and bench to bedside. Brain Research, 1293, 2-12.

5. Suicidal behaviors and predictive modeling. Army STARRS (2009-2015) and STARRS-LS (2014-2019) were designed to comprehensively examine the mental health and resilience of Soldiers, and is the largest research study ever conducted among military personnel. One of the studies was an historical cohort study of more than 1.6 million Soldiers on active duty from 2004-2009. The Army STARRS/STARRS-LS research includes questionnaires, neurocognitive tests, blood collection, state-of-the-art genetic and other biomarker assays, and linking these data to existing Army/DoD records, producing large and risk datasets to serve the goals of the study as well as broader goals involving other mental health outcomes.
a). Kessler, R. C., Stein, M. B., Petukhova, M. V., Bliese, P., Bossarte, R. M., Bromet, E. J., Fullerton, C. S., Gilman, S. E., Ivany, C., Lewandowski-Romps, L., Bell, A. M., Naifeh, J. A., Nock, M. K., Reis, B. Y., Rosellini, A. J., Sampson, N. A., Zaslavsky, A. M., Ursano, R. J., & Army STARRS Collaborators (2017). Predicting suicides after outpatient mental health visits in the Army Study to Assess Risk and Resilience in Servicemembers (Army STARRS). Molecular Psychiatry, 22(4), 544-551. doi: 10.1038/mp.2016.110
b) Ursano, R. J., Kessler, R. C., Stein, M. B., Naifeh, J. A., Nock, M. K., Aliaga, P. A., Fullerton, C. S., Wynn, G. H., Ng, T. H. H., Dinh, H. M., Sampson, N. A., Kao, T. C., Schoenbaum, M., McCarroll, J. E., Cox, K. L., & Heeringa, S. G., on behalf of the Army STARRS collaborators (2016). Medically documented suicide ideation among U.S. Army Soldiers. Suicide & Life-Threatening Behavior. doi: 10.1111/stlb.12316
c) Ursano, R. J., Kessler, R. C., Herringa, S. G., Cox, K. L., Naifeh, J. A., Fullerton, C. S., Sampson, N. A., Kao, T., Aliaga, P. A., Vegella, P. A., Mash, H., Buckley, C., Colpe, L. J., Schoenbaum, M., & Stein, M. B. (2015). Non-fatal suicidal behaviors in U.S. Army administrative records, 2004-2009: Results from the Army Study to Assess Risk and Resilience in Servicemembers (Army STARRS). Psychiatry, 78(1), 1-21. doi: 10.1080/00332747.2015.1006512
d) Nock, M. K., Stein, M. B., Heeringa, S. G., Ursano, R. J., Colpe, L. J., Fullerton, C. S., Hwang, I., Naifeh, J. A., Sampson, N. A., Schoenbaum, M., Zaslavsky, A. M., & Kessler, R. C. (2014). Prevalence and correlates of suicidal behavior among soldiers: Results from the Army Study to Assess Risk and Resilience in Servicemembers (Army STARRS). JAMA Psychiatry, 71(5), 514-522.

Bachelor of Science (December 1985)
Major: Zoology
University of Texas at Austin

Doctor of Philosophy (May 1991)
Field of Study: Physiology of Reproduction
Texas A&M University
College Station, TX

Postdoctoral Fellow (1991 - 1994)
Field of Study: Neuroendocrinology
Columbia University
New York, NY

Postdoctoral Fellow (1994 - 1999)
Field of Study: Molecular Neuroendocrinology
Mount Sinai School of Medicine
New York, NY

He graduated for Shanghai Medical University in 1976 and was a psychiatry resident at Department of Psychiatry of Shanghai Medical University from 1977-1980, and a senior staff fellow at Behavioral and Endocrinology Branch of NIMH, NIH between 1992-2001.

The ultimate goal of Dr. Zhang’s research is to acquire and provide the knowledge that is necessary for the development of novel and effective molecular tools for stress-related diseases such as PTSD. His laboratory is dedicated to elucidating the molecular and cellular mechanisms of the actions of genes such as p11 (S100A10), FKBP5, BDNF, and mitochondria focused-genes in stress, PTSD, The long-term goal is to establish a molecular basis from which the lab can search for a therapeutic target or biomarker for PTSD and suicide risk. Previously, they found that P11 is associated with PTSD. Its mRNA levels are increased in the post-mortem prefrontal cortex (area 46) of PTSD patients. Stress-induced p11 over expression in the prefrontal cortex (PFC) accompanied by elevation of corticosterone concentration in the blood was also observed in rats subjected to three days of inescapable shock. Their mechanism study demonstrated that through glucocorticoid response elements (GREs) within the p11 promoter, dexamethasone (Dex), a synthetic glucocorticoid, up-regulates p11 expression, which can be attenuated by either a glucocorticoid receptor antagonist, RU486, or mutating two of the three GREs. Later in their translational study, they found that levels of p11 as a potential biomarker in peripheral blood distinguish patients with PTSD from those with other major psychiatric disorders including bipolar depression, major depressive disorder, and schizophrenia. His research program has undertaken the following specific objectives:
1. To identify gene networks or pathways of PTSD.
2. To investigate the novel molecular regulatory mechanism of stress and PTSD in vivo and in vitro. His research will provide useful information, which might help translational research, from bench to bed.