April, 2012
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Society of Biological Psychiatry
 
"Scientists collaborating to eliminate the suffering of mental illness."
In This Issue
SOBP Vision Statement
Message from the Editor
2012 Meeting Announcement
Officer Elections
Journal Updates
Welcome New Members
Other Meetings of Interest
Get Involved
SOBP Contact Information
SOBP Vision Statement

The vision of the Society of Biological Psychiatry is to integrate, advance, and promulgate science relevant to psychiatric disorders, in order to reduce or prevent the suffering of people with these conditions.

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Message from the Editor

Strakowski picture with monitor

Well, it's spring time again, when our thoughts turn to sunshine, warm weather, love and the SOBP annual meeting (and mania, for those of us interested in bipolar disorder)! This year's meeting focuses on systems neuroscience, an emerging approach for thinking about brain function that appears to be an ideal fit for studying and modeling mental disorders. Throughout the past few decades, we have increasingly learned that reducing human behaviors and behavioral disorders to single brain regions fails to represent the complexity of the neural underpinnings of these conditions. In order to understand mental illnesses, we must understand how brain circuits and networks integrate to modulate emotional, social, and cognitive behaviors. This year's annual meeting is designed to initiate that process. Additionally, last year, we announced that we were hoping to shift our paradigms of models for mental disorders, so that this year the SOBP annual meeting presents an opportunity to make this shift. To that end, the first plenary session takes a systems neuroscience approach toward understanding the neurochemistry of social behavior, how social neuroscience helps us think about race and ethnicity, and how social cognition contributes to learning and development. For those of us with teenagers, Dr. Blakemore's discussion of the social brain in adolescence may be particularly relevant (I consider my own pre-adult sons as humanized chimpanzees, at least at times, to better understand their behavior, something of systems-neuroscience approach I suppose). On the second day, we will then explore neuroimaging techniques and applications toward thinking about brain networks, to extend the value of these approaches from our more standard 'Region of Interest" thinking. Finally, on the last day a two-part plenary first helping us think about reward systems (rather than reward regions) and the novel application of iPS cells in schizophrenia and autism, round out a challenging series of lectures to encourage novel approaches to studying behavioral conditions. The program committee has complemented these outstanding plenary sessions with exciting new work across the field of psychiatry and behavioral neuroscience. There is little doubt that this year's annual meeting will provide a premier opportunity to improve our research and scholarly work and thinking. I hope to see you all there. Please read through this newsletter for additional information, dates and deadlines for this meeting.

 

Best Wishes

Steve Strakowski, MD
Senior Associate Dean for Research

UC Health Vice President for Research

Professor and Chair, Department of Psychiatry & Behavioral Neuroscience

  

2012 Annual Meeting - Important Announcements 

 

Society of Biological Psychiatry's 67th Annual Meeting

May 3-5, 2012

Sheraton Philadelphia Downtown Hotel

Philadelphia, Pennsylvania

 


We are only 2 weeks away from the annual meeting.  Register now and don't miss the opportunity to participate, network and engage with your colleagues.
 
Meeting Registration - April 20, 2012 Deadline:
  •  If you haven't already registered, please do so before the April 20th deadline.  We will accommodate on-site registration but after April 20th, the fees will increase by $100, so register on-line now or before April 20th and save $$$'s.  If you have any questions regarding your registration, email sobp@sobp.org.  

Hotel Reservations:

  • You should already have your hotel room reserved. 
  • Our convention hotel, the Sheraton Philadelphia Downtown Hotel is sold out as well as our overflow hotel at the Embassy Suites.  
  • We have a block of rooms available at the  Radisson Plaza - Warwick Hotel just a short walk from the Sheraton.  
Program Materials:
  • Abstract Supplement
    • The abstract supplement will be mailed to members prior to the meeting as a supplement to their journal subscription to Biological Psychiatry
    • Non-members will receive the abstract supplement at the SOBP registration desk.
  • On-Line Program Planner 
    • View the entire program including late-breaking abstracts and create your own itinerary for the meeting.     
  • Ebook
    • The electronic copy of the abstract book is available to download to your ebook or smart phone to search for information, mark abstracts, and make notes using Ebook technology.    
  • Program Book & Meeting-at-a-Glance
    • Will be provided to all attendees upon check in at the SOBP Registration Desk 

Visit the SOBP meeting website for up-to-date information regarding the meeting.  For questions, email sobp@sobp.org.

 

See you in Philadelphia 

 

Invitation to McLean Hospitals Reception at APA Meeting
You are invited to the McLean Hospital's Reception at the APA Meeting 

Sunday, May 6th, 6 pm to 8 pm 

The Franklin Institute

RSVP by April 30th 

 

In the spirit of inquiry embodied by Benjamin Franklin, McLean Hospital President and Psychiatrist in Chief Scott L. Rauch, MD, invites you to join him during the American Psychiatric Association Annual Meeting in Philadelphia for an exciting evening of cocktails, music, science and technology.

 

Officer Elections
The Society of Biological Psychiatry announces the election for President and Councilor-at-Large.  The Society is pleased to announce the following slate of candidates:

President:
John G. Csernansky, MD
Ned H. Kalin, MD

Councilor-at-Large
Daniel C. Javitt, MD, PhD
Myrna M. Weissman, PhD

One of the most important benefits and responsibilities of Society membership is voting for the Board of Directors and other important issues.  As voting members of the Society please exercise your membership benefit and cast your vote by Monday, April 30, 2012. Results will be announced in May, 2012.
Journal Updates

 

Journal Cover

Important Findings Published in Biological Psychiatry

By Caleb M. Adler, MD.  

 

January 15, 2012

 

Commentary by Aysenil Belger, Gunes H. Yucel, and Franc C.L. Donkers

Atkinson RJ, Michie PT, Schall U (2012). Duration mismatch negativity and p3a in first-episode psychosis and individuals at ultra-high risk of psychosis. Biol Psychiatry 71:98-104

Patients with schizophrenia have been observed to display reduced mismatch negativity (MMN), an early negative ERP component seen in response to discriminable changes in repetitive auditory stimuli. MMN have been separated into components, some of which may be more prominent in varying disease states and chronicity. In this paper, the authors measured MMN and P3a, an ERP component reflecting attentional reorientation, in subjects at "ultra-high" risk of psychosis (UHR), subjects having their first psychotic episode (FEP), and healthy controls. Ultra-high risk subjects are "clinically high risk" (CHR) individuals, defined by at least some prodromal symptoms. The authors found that MMN and P3a were reduced in both UHR and FEP subjects, at least at the trend level. They noted that these findings suggest that MMN and P3a are reduced very early in the course of illness and might represent potential prodromal markers. In the commentary, the potential relationship between MMN and the pathophysiology of schizophrenia is reviewed. The commentary authors note the importance of studying early disease markers but point out that in the absence of longitudinal follow-up, one cannot conclude that findings in CHR individuals are not markers of subsyndromic pathology rather than predictors of future pathology.

Commentary by Michael F. Green and Junghee Lee

Taylor SF, Kang J, Brege IS, et al (2012). Meta-analysis of functional neuroimaging studies of emotion perception and experience in schizophrenia. Biol Psychiatry 71:136-145

In this paper, the authors describe their meta-analysis of functional imaging studies of emotion in patients with schizophrenia. The authors subdivide the available data in several ways to separately address specific aspects of emotional experience. They report that emotional perception is associated with decreased activity in schizophrenic patients throughout much of the expanded limbic network, including amygdala/hippocampus, portions of the prefrontal cortex, and subcortical structures. Schizophrenic patients showed increased activity in other regions, suggested to be compensatory in nature. The authors further describe differences in findings during implicit emotion tasks, in which subjects typically viewed emotion-inducing stimuli (e.g. faces) and explicit tasks, during which subjects were called upon to take a more active role-- noting in particular that areas of increased activation with schizophrenia were seen only during the latter. In the commentary, Drs. Green and Lee suggest some interpretations of these findings in light of previous work, as well as offering some cautionary notes. 

 

February 1, 2012  

 

Commentary by Wolfram Schultz

Sugam JA, Day JJ, Wightman RM, et al (2012). Phasic nucleus accumbens dopamine encodes risk-based decision-making behavior. Biol Psychiatry 71:199-205

The authors examined dopamine release in the nucleus accumbens (NAc) of a small group of rodents trained on a risk-based decision-making task. Rats showed individual-specific preferences for risk-taking or risk-avoidant behavior that was reflected in dopamine release during choice and forced-choice trials. These findings suggest a role for dopamine projections to the NAc in risk-related decision making. The commentary expands on the manuscript by reviewing the cognitive nature of risk and current findings linking risk-related decision making to dopaminergic activity. Potential follow-up studies are discussed as well.

Commentary by Scott J. Russo

Wei Q, Fentress HM, Hoversten MT, et al (2012). Early-life forebrain glucocorticoid receptor overexpression increases anxiety behavior and cocaine sensitization. Biol Psychiatry 71:224-231

In this elegant experiment, Wei and colleagues address the importance of timing to the relationship between forebrain glucocorticoid receptor (GR) over-expression and emotional reactivity. The investigators show that in a mouse line with inducible GR over-expression, transient over-expression during early life led to increased behavioral effects. In contrast, post-weaning over-expression was not associated with similar outcomes. Early over-expression was also associated with long-term changes in transcription patterns. In the commentary, the role of glucocorticoids in stress response is reviewed. Dr. Russo observes that this manuscript extends current understanding of potential mechanisms underlying the effects of glucocorticoids on stress response, and suggests both further research avenues and potential therapeutic applications.

 

February 15, 2012      

 

Commentary by Joan Kaufman

Dannlowski U, Stuhrmann A, Beutelmann V, et al (2012). Limbic scars: long-term consequences of childhood maltreatment revealed by functional and structural magnetic resonance imaging. Biol Psychiatry 71:286-293

The investigators obtained structural and functional magnetic resonance images from a large group of healthy adults. All subjects were screened for childhood trauma. The investigators report that exposure to traumatic events in childhood, reflected in scores on the Childhood Trauma Questionnaire (CTQ) was associated with amygdala activation in response to threatening faces, presented as part of a face-matching paradigm. High CTQ scores were further associated with reduced gray matter volume in prefrontal, medial temporal and subcortical structures including the insula, orbitofrontal cortex, anterior cingulate, hippocampus, and caudate. The authors note that these findings are consistent with studies of patients with depression and PTSD, suggesting that these functional and structural changes may be mediators between adverse childhood events and the appearance of later psychopathology.

Nikulina V, Widom CS, Brzustowicz LM (2012). Child abuse and neglect, MAOA, and mental health outcomes: a prospective examination. Biol Psychiatry 71:350-357

The investigators recruited a large number of adults with substantiated history of child abuse and neglect, as well as a matched comparison group. All participants were genotyped for monoamine oxidase A (MAOA) alleles. The MAOA encodes for an enzyme involved in the elimination of monoamine neurotransmitters, and has been identified as a moderator between childhood stress and longer term outcomes. The investigators found that a low-activity genotype decreased dysthymia in abused and maltreated women; and was associated with decreased risk of dysthymia, depression and alcohol abuse in white participants who had been sexually abused. In contrast, the high-activity genotype was protective in non-white (predominantly African-American) individuals. In the commentary, Dr. Kaufman comprehensively reviews genetic influences, and particularly the possible role of the MAOA gene in moderating between childhood abuse and the appearance of psychopathology.

Commentary by Elisabeth B. Binder and Florian Holsboer

Lovallo WR, Farag NH, Sorocco KH, et al (2012). Lifetime adversity leads to blunted stress axis reactivity: studies from the Oklahoma Family Health Patterns Project. Biol Psychiatry 71:344-349

The investigators tested 354 healthy young adults using a version of the Trier Social Stress Test (TSST) in which subjects were asked to engage in public speaking and mental arithmetic in front of a panel. Subjects were stratified by the number of sign infant adverse life events they had previously experienced, ranging from zero to four. The investigators report that previous adverse events were associated with lower heart rates and cortisol response to the stress task across gender. They note that their findings support previous suggestions that early life events may have a significant impact on reactivity to stress. In the commentary, these findings are discussed and potential explanations explored.

Commentary by Jacek Dębiec

Schwabe L, Nader K, Wolf OT, et al (2012). Neural signature of reconsolidation impairments by propranolol in humans. Biol Psychiatry 71:380-386

The investigators sought to test whether the β-adrenergic receptor antagonist, propranolol would interfere with the reconsolidation of recalled negative emotional pictures by altering medial temporal activity. Healthy individuals were exposed to neutral and emotional pictures and subsequently participated in an fMRI scan during which they were asked to recall the pictures-some after receiving propranolol. Subjects later participated in another fMRI scan during which they performed a recognition task around the same pictures. The investigators report that propranolol reduced subsequent memory for emotional pictures. Further, propranolol administration was associated with increased medial temporal activity during recall of recognized pictures. The commentary discusses the role of norepinephrine in memory consolidation and reconsolidation in light of previous preclinical and clinical studies. The findings of Schwabe and colleagues are further reviewed with particular emphasis on some seemingly paradoxical results and possible explanations for these data.

 

March 1, 2012   

 

Commentary by Jennifer G. Mulle and Stephen T. Warren

Fernandez TV, Sanders SJ, Yurkiewicz IR, et al (2012). Rare copy number variants in tourette syndrome disrupt genes in histaminergic pathways and overlap with autism. Biol Psychiatry 71:392-402

The authors studied copy number variants (CNV) in patients with Tourette Syndome (TS) as well as healthy controls. Individuals with TS did not differ from controls in number of de novo or transmitted rare CNVs. Nonetheless, the TS patients did show non-significantly larger rare CMVs, as has been found in other psychiatric disorders. Further evaluation of rare CMVs suggested the involvement of genes implicated in several psychiatric disorders, including genes involved in histaminergic neurotransmission. The commentary notes the importance of these findings to hypotheses of shared risk between developmental disorders.

 

March 15, 2012  

 

Commentary by Michael D. Ehlers

Cavus I, Reinhart RM, Roach BJ, et al (2012). Impaired visual cortical plasticity in schizophrenia. Biol Psychiatry 71:512-520

The investigators build on previous studies of cortical plasticity that have identified abnormalities in patients with schizophrenia, using visual evoked potentials to measure long-term potentiation (LTP), a form of neuroplasticity. Visual evoked potentials (VEP) were elicited from healthy controls and patients with schizophrenia using a series of stimuli designed to evoke VEP potentiation as part of an odd-ball paradigm. Two negative-voltage components were identified in a principal components analysis, and compared between groups. The investigators found significant differences between schizophrenic patients and healthy controls indicative of impaired visual cortical plasticity in the former group.

Clapp WC, Hamm JP, Kirk IJ, et al (2012). Translating long-term potentiation from animals to humans: a novel method for noninvasive assessment of cortical plasticity. Biol Psychiatry 71:496-502

The authors synopsized and discussed their previous research demonstrating that repetitive sensory stimuli may induce long term potentiation that may be measured with EEG and fMRI. They further present evidence that LTP in humans is homologous with synaptic LTP observed in preclinical experiments, and discuss potential clinical applications of these findings.

Cooke SF, Bear MF (2012). Stimulus-selective response plasticity in the visual cortex: an assay for the assessment of pathophysiology and treatment of cognitive impairment associated with psychiatric disorders. Biol Psychiatry 71:487-495

The authors describe stimulus-specific response potentiation (SRP), an example of experience-dependent plasticity observed in the visual cortex of rodents in response to repeated visual stimuli. They present evidence that SRP represents a form of long-term potentiation involving thalamo-cortical synaptic transmission. They further describe potential clinical utility of SRP, particularly in patients with schizophrenia.

Mears RP, Spencer KM (2012). Electrophysiological assessment of auditory stimulus-specific plasticity in schizophrenia. Biol Psychiatry 71:503-511

The authors used event-related potentials (ERP) to measure neuroplasticity in schizophrenic patients and healthy controls in response to an auditory odd-ball task. They reports significant differences in response that suggest abnormal auditory neuroplasticity in the former group. They further suggest that these methods may be clinically useful for developing novel therapeutics for schizophrenia.  The commentary reviews the legacy of long-term potentiation research in psychiatry, and places the findings of the four studies reviewed into that larger context. Dr. Ehlers notes that the four articles suggest methodologies to facilitate non-invasive assessment of LTP, and suggest the presence of LTP abnormalities in patients with schizophrenia. The commentary goes on to discuss the potential role for these techniques in clinical psychiatry as bio-markers and in advancing our understanding of the underlying neuropathology of psychiatric illnesses thought to involve abnormalities in neural circuitry.

 

Members of SOBP receive Biological Psychiatry as part of their membership     Click here to learn more about this prestigious journal.

 

Top 6 Reasons to Publish in Biological Psychiatry  
1.  High Impact Factor - 8.674
2.  4th of 126 Psychiatry Journals
3.  15th of 237 Neuroscience Journals
4.  1st Decision - 30 Days
5.  ePubs - 6 Weeks
6.  In Print - 4 Months
Welcome New Members
Please welcome the following new members to the Society, approved April 1, 2012

 

Name

Institution

Murat Ilhan Atagun

Selcuk University - Turkey

Nancy M. Bivens

Columbia University

Joseph Boscarino

Geisinger Clinic

Brett Clementz

University of Georgia

Elise M. Demeter

University of Michigan

Teresa Franklin

University of Pennsylvania

Justine Gatt

University of Sydney Medical School

Polaris Gonzalez

Ponce School of Medicine - Puerto Rico

Sarah Grimwood

Pfizer, Inc.

Adam Guastella

University of Sydney - Australia

Neil Harrison

University of Sussex - UK

Howard Hassman

CRI Lifetree

Theresa Jacob

Maimonides Medical Center

Emily Goard Jacobs

University of California San Francisco

Ana Liso Navarro

University of Massachusetts Medical School

Rodrigo Machado-Vieira

University of Sao Paulo - Brazil

Donald A. Malone

Cleveland Clinic

Kevin Malone

University College/Dublin

Ketan Marballi

University of Texas Health Science Center

Marie-Laure Paillere Martinot

Cochin Hospital, Paris

Frank Menniti

Mnemosyne Pharm. Inc.

Jeffrey M. Miller

Columbia University

Rajendra Morey

Duke University

Kelly A. Newell

University of Wollongong - Australia

Kerry J. Ressler

Emory University

David Roofeh

University of Pittsburgh Medical School

Takeshi Sakurai

Medical Innovation Center/Kyoto University - Japan

Carl Schwartz

Massachusetts General Hospital

Gen Shinozaki

University of South Dakota

James Shoblock

Janssen Research & Development Co.

Peter Siekmeier

McLean Hospital

Elif M. Sikoglu

University of Massachusetts Medical School

Ravi Singareddy

Penn State University College of Medicine

Rajita Sinha

Yale University School of Medicine

Rebecca Sripada

University of Michigan

Paul G. Unschuld

Johns Hopkins School of Medicine

Aristotle Voineskos

University of Toronto

David W. Volk

University of Pittsburgh

Mohammed A Warsi

McMaster University

Leslie Winter

Aurora Mental Health Center


If you are interested in joining the Society please visit www.sobp.org or email sobp@sobp.org.  We will be happy to answer any questions you may have regarding the Society or find a sponsor for your application. 
Other Meetings of Interest

International Society for Affective Disorders Conference 

April 18-20, 2012

Royal College of Physicians 

London

 

1st Istanbul-Eurasian Regional Congress of Biological Psychiatry 

May 17-31, 2012

Istanbul, Turkey

 

52nd NCDEU Meeting

May 29 - June 1, 2012

Arizona Biltmore Resort & Spa 

 

XXth World Congress of Psychiatric Genetics: Confronting the Complexity of Brain and Behavior 

October 14-18, 2012

Hamburg, Germany

 

A Joint Congress of Psychiatry 

November 29 - December 2, 2012

Athens, Greece

  • World Psychiatric Association Thematic Conference on Intersectional Collaboration: The Multidisciplinary Facets of Psychiatry
  • Fourth European Congress of the International Neuropsychiatric Association: Overlap and Integration in Neuropsychiatry
  • First Interdisciplinary Congress on Psychiatry and Related Sciences

ACNP Annual Meeting 

December 2-6, 2012
The Westin Diplomat

Hollywood, Florida

 

May 23-27, 2013
Kyoto, Japan


 

Get Involved
Want to be engaged and involved with one of our committees? Looking for a leadership opportunity?  Then signup to join one of the Society's many award committees or a task force.  Click here to tell us which groups you would be interested in joining.
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SOBP's Career Center connects our members with employment opportunities and employers with the best professionals within our membership. Employment opportunities range from post-doc positions, faculty positions, neuroscience jobs in industry and alternative careers.
 
Visit SOBP's Career Center  today to explore employment opportunities.  Post an anonymous resume for employers or recruiters to view.
 
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Contact Us
Society of Biological Psychiatry Business Office
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Jacksonville, FL 32224
904-953-2842 Office
904-953-7117 Fax
 
Biological Psychiatry Editorial Office
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214-648-0880 Office
214-648-0881 Fax
Society of Biological Psychiatry Newsletter Editorial Staff 

Stephen M. Strakowski, MD, Editor

Editorial Board
Helen Mayberg, MD
William B. Lawson, MD, PhD, DLFAPA 
Alan H. Young, MD, PhD
Caleb M. Adler, MD
904-953-2842
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