October, 2011
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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
Welcome New Members
NIMH Administrative Supplement Program
Biological Psychiatry New Website
Journal Updates
2011 Annual Meeting Recordings
Membership Renewals
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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In This Issue 

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Message from the Editor

Strakowski picture with monitor Do We Need a DSM-V?


Recently, psychiatric diagnosis is on our minds with DSM-V committees in full swing. In my view, a diagnosis is used to isolate a 'case' from the general population for three primary reasons: 1) to define a treatment that will alleviate suffering; 2) to predict outcome (prognosis); and 3) to facilitate research into illness etiology. With these considerations in mind, do we need a DSM -V?


The Diagnostic and Statistical Manual: Mental Disease (DSM-I) originated in 1952. DSM-II expanded this volume and was published in 1968. In both publications, descriptions of psychiatric conditions were dominated by psychodynamic and psychoanalytic conceptualizations of most psychiatric conditions (Grob AJP 1991; 148:421-431). Because these DSM-I and II categorizations were difficult to operationalize, they were of limited value for medical research; moreover they did not gel with the International Disease Classification (ICD), and frankly did not sufficiently address the three reasons for making a diagnosis in the first place. Consequently, DSM-III (1980) was developed to address these shortcomings. DSM-III re-conceptualized psychiatric disorders into a medical-research model (Wilson M. AJP 1993; 150:399-410), revolutionizing psychiatric nomenclature and invigorating neuroscience approaches to psychiatric research. Many of these diagnoses were useful for defining treatment and predicting outcome, although discoveries of etiologies have remained elusive. DSM-III was revised in 1987 (DSM-III-R) and again in 1994 (DSM-IV, and DSM-IV-TR). Significant changes in diagnostic criteria occurred with each revision, largely to make the DSM more 'user-friendly' for clinicians and address concerns raised about being both overly narrow and too vague when "pathologizing" behavior. However, few studies were performed to determine whether changes in diagnostic criteria improved: 1) our ability to predict treatment response; 2) our ability to predict outcome; or 3) our ability to define etiologies. As we face DSM-V then, has sufficient new information arisen to warrant changes in diagnostic criteria yet again? In short, the answer is: No.


So what harm is there in prematurely altering diagnostic criteria? Indeed, from a clinical viewpoint, such changes might open treatment options for people who might otherwise not receive them and may therefore benefit. Are we not trying to do exactly this? Unfortunately, in the absence of treatment data justifying a criteria change, people are just as likely to be exposed to ineffective treatments and unnecessary side-effects. Prognostic data take years to accumulate, typically longer than between each revision of DSM. Consequently, another revision will simply restart and delay this incomplete process. Whether proposed changes will facilitate studies into the etiologies of the newly defined syndromes is not known, but previous revisions have not exhibited such successes in the past. Finally, with each revision, the number of diagnosable conditions increases. With each increase, psychiatry is criticized for 'creating' diagnoses to: 1) increase revenue to clinicians; 2) partner with big pharma to expand the mental health market; or 3) simply raise money for the DSM publishers. Consequently, in the absence of research demonstrating that new definitions meaningfully advance the utility of our diagnoses, our credibility with the public and our medical colleagues is challenged with each DSM revision. Only when we first accumulate research supporting changes in our diagnostic systems will we meet these challenges effectively. We are not at this point now.


With this said, there are very good, smart, and thoughtful people involved with the creation of DSM-V, who likely disagree with me. I welcome comments on this editorial and will publish thoughtful responses in the next newsletter.    


Or, continue the discussion at the newly formed Society of Biological Psychiatry LinkedIn Group, created to foster discussions on topics of interest to the community.  Join the group, invite others, and continue the discussion.


Thank you.


Stephen M. Strakowski, MD

Senior Associate Dean for Research, UCCOM

Vice President of Research, UC Health 

The Dr. Stanley and Mickey Kaplan Professor and Chairman

Dept. of Psychiatry, University of Cincinnati


2012 Annual Meeting - Important Announcements 


Society of Biological Psychiatry's 67th Annual Meeting

May 3-5, 2012

Sheraton Philadelphia Downtown Hotel

Philadelphia, Pennsylvania



 Important Dates

       September 1, 2011 - Abstract Submission Opens
October 24, 2011 - Overall Symposium Proposal Due

October 31, 2011 - Individual Symposium Abstracts Due 

December 12, 2011 - Oral and Poster Abstracts Due

January 9, 2012 - Hotel and Meeting Registration Opens

February 20, 2012 - Late Breaking Abstract Submission Opens*

March 16, 2012 - Late Breaking Abstracts Due*

April 20, 2012 - Registration Closes

 *Tentative Dates - Subject to Change


Submit Your Abstract Now

Symposium Submission Site (Deadline October 24, 2011)

Oral or Poster Submission Site (Deadline December 12, 2011)


2012 Annual Meeting Awards

The Society is pleased to offer the following awards, including a limited number of travel fellowship awards.  Submit your applications for these awards by November 30, 2011.  Award recipients will be announced in January, 2012.  Visit www.sobp.org for additional information and to submit your application. 


Travel Fellowship Award - Domestic Applicants

Travel Fellowship Award - International Applicants

Ziskind-Somerfeld Research Award (Nominations provided by journal office)

A. E. Bennett Research Awards

George N. Thompson Award for Distinguished Service

Gold Medal Award

Humanitarian Award


Members Must Sponsor Abstract Submissions 

Non-members will need a member in good standing of the Society to sponsor their abstract submissions.  Members need only to allow their name to be used on the abstract submission.   If you do not know a member and need a sponsor for your abstract, email sobp@sobp.org.  We will find a sponsor for you.    Members - when asked to sponsor an abstract, take a moment to explain why you joined the Society and encourage the non-member to consider joining the Society of Biological Psychiatry.  There is no limit to the number of abstracts a member may sponsor and you do not need to be a co-author on the abstract.   


Visit www.sobp.org for the preliminary program and to submit a symposium proposal or oral or poster abstract.   For questions, email sobp@sobp.org.

Elections for Officers and Changes to Constitution & By-Laws
Officer Elections
It is time to elect your new President and Councilor-at-Large.  We are pleased to present these distinguished members for the following positions:

For President (2012-2013)
Judith M. Ford, MD
Scott L. Rauch, MD

For Councilor-at-Large (2011-2014)
Linda L. Carpenter, MD
Daniel C. Javitt, MD, PhD 

Constitution and By-Laws
It has been a few years since the Society's Constitution and By-Laws have been updated.  Council has reviewed and made several changes which will better support the organization and mission of the Society.  Most changes are simply clarification to the existing language or changes to the format of the document for ease of reading.  However, there are a few major changes to note:
  1. A new Student Member category has been created.  This category will address the needs of students who want to become a member of the Society. 
  2. The Corresponding Member category has been eliminated.  Members living outside North America may continue to join as a Regular Member of the Society.  Current Corresponding Members may convert their membership to a Regular Member.    
  3. Memberships will be reviewed and approved on a more frequent basis allowing new members to quickly become engaged with the Society.    

All voting members will receive an email with a link to cast your vote.  The email will contain more detailed explanation of these changes along with the revised Constitution and By-Laws.  Look for your ballot in your email by October 10th.   

Welcome New Members
Please welcome the following new members to the Society.  These members were approved September 2011. 

Hadar Ben-Yoav - University of Maryland

Christopher Cain - Nathan Kline Institute for Psychiatric Research/NYU
Kristina Deligannadis - University of Massachusetts
Irina Esterlis - Yale University
Shao-Hsuan Ho - University of Michigan
Jennifer Hoblyn - VA Palo Alto Health Care System
Robert Kessler - University of Toronto
Linda Mah - Rotman Research Institute
Kristen O'Hearn - University of Pittsburgh School of Medicine
Kazi Rahman - California Department of Correction
Paul Shepard - Maryland Psychiatric Research Center
Gustavo Turecki - McGill University

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. 
NIMH Administrative Supplement Program
A new NIMH program may be of interest to the SOBP membership.  This NIMH administrative supplement program (see NOT-MH-11-014) will provide opportunities for MD/PhDs to conduct research and enhance their research skill set while completing clinical training (i.e. during residency and clinical fellowship).  The limited availability of options to support research effort during clinical training is seen as a significant barrier to increasing the pipeline of outstanding MD/PhDs who are prepared to conduct innovative, NIMH-supported research.  This administrative supplement program begins to address this barrier.  We hope it will facilitate continued research by MD/PhDs during clinical training and enable their efficient transition to research independence shortly thereafter.  This program provides funds as an administrative supplement to an active research grant (see NOT-MH-11-014 for details).  Information about eligibility, selection factors, budget, and how to apply are found in the Notice.  Potential applicants are encouraged to contact one of the Program staff listed in NOT-MH-11-014 so that any questions may be addressed before an application is submitted.  
Biological Psychiatry Releases New Website

Biological Psychiatry is proud to announce the release of their updated website.  


The web address remains the same, www.sobp.org/journal, but visitors will notice an improved visual layout, enhanced features, and greater functionality. The home page is now much more user-friendly to quickly find the features you're looking for, whether you'd like to access the current Table of Contents, view Articles in Press, or find information on submitting a paper. You can also easily sign-up to receive free electronic Table of Contents alerts.


Individual articles are have also undergone a significant re-design. In addition to an improved full-text layout, readers can also e-mail selected abstracts, download figures to PowerPoint, and view citation data.


With its bi-monthly publication schedule, the site is updated frequently so check back often. Additional tweaks are still underway, and a web-only journal feature that highlights editors' picks will be added soon.


As always, the journal welcomes your feedback. Feel free to contact them at biol.psych@utsouthwestern.edu.  

Journal Updates


Journal Cover

Important Findings Published in Biological Psychiatry

By Caleb M. Adler, MD.  


July 1, 2011 


Commentary by Thomas R. Insel, Sarah E. Morris, and Robert K. Heinssen

Carter CS, Barch DM, Bullmore E, et al (2011). Cognitive neuroscience treatment research to improve cognition in schizophrenia II: developing imaging biomarkers to enhance treatment development for schizophrenia and related disorders. Biol Psychiatry 70:7-12  

In this review article, the authors give an overview of the first meeting of the second phase of the "cognitive neuroscience treatment research to improve cognition in schizophrenia." This meeting was concerned with exploring issues around the use of neuroscience techniques such as functional magnetic resonance imaging (fMRI), electroencephalography (EEG), magnetoencephalography (MEG), and transcranial magnetic stimulation (TMS). Later articles discuss the use of each of these techniques as biomarkers for treatment development.

Barch DM, Mathalon DH (2011). Using brain imaging measures in studies of procognitive pharmacologic agents in schizophrenia: psychometric and quality assurance considerations. Biol Psychiatry 70:13-18  

In the article, the authors review psychometric issues that need to be considered in applying potential biomarkers to the process of drug discovery. In particular, the authors focus on multiple aspects of both reliability and quality assurance. The issues broached are widely applicable to a variety of psychiatric disorders and imaging modalities.

McClintock SM, Freitas C, Oberman L, et al (2011). Transcranial magnetic stimulation: a neuroscientific probe of cortical function in schizophrenia. Biol Psychiatry 70:19-27  

While the clinical utility of transcranial magnetic stimulation (TMS) is briefly reviewed, the article largely focuses on the use of TMS in conjunction with electrophysiological and functional imaging modalities. Potential TMS research paradigms are reviewed at length, and the authors conclude that TMS is a useful probe of cortical function and might serve to help identify potential biomarkers in the future.

Luck SJ, Mathalon DH, O'Donnell BF, et al (2011). A roadmap for the development and validation of event-related potential biomarkers in schizophrenia research. Biol Psychiatry 70:28-34  

In this article, the authors address the use of event-related potential (ERPs) as possible biomarkers. To place this discussion in context, Dr. Luck and colleagues review the neurophysiology of ERPs at some length before discussing application of ERPs as a potential biomarker of treatment for psychiatric illness. While the strengths of this technique are noted, the authors also discuss aspects of the technique that will need to be addressed prior to wide-spread implementation.


July 15, 2011 


Commentary by Ola Sternäng and Åke Wahlin

Taylor AE, Guthrie PA, Smith GD, et al (2011). IQ, educational attainment, memory and plasma lipids: associations with apolipoprotein E genotype in 5995 children. Biol Psychiatry 70:152-158

Apolipoprotein E (APOE) genotype has been previously found to be associated with lipid levels, and with Alzheimer's disease in older adults. In this paper, the authors examined the relationship between apolipoprotein E (APOE) genotype and plasma lipids, IQ, and school performance in a large cohort of children. Dr. Taylor and colleagues found that APOE genotype was associated with measures of plasma lipids, but in contrast to older adults there was no relationship with IQ or school performance. In their commentary, Drs. Sternäng and Wahlin discuss the uniqueness of this study but note that some pertinent cognitive domains were not addressed, and that studying interactions between multiple factors such as lipids, cognition and gender might be useful in further elucidating the role of APOE genotype in cognitive decline.

Commentary by Francis Lotrich

Capuron L, Schroecksnadel S, Féart C, et al (2011). Chronic low-grade inflammation in elderly persons is associated with altered tryptophan and tyrosine metabolism: role in neuropsychiatric symptoms. Biol Psychiatry 70:175-182  

A number of recent studies have linked peripheral inflammatory processes to the development of mood symptoms. In this paper, the authors identify some potential pathways for interactions between inflammation and the biosynthesis of monoamines. The authors report evidence of indoleamine-2,3-dioxygenase (IDO) induced increases in tryptophan catabolism, as well as changes in neopterin and nitrite levels, and in the phenylalanine/tyrosine ratio, consistent with inflammatory effects on the guanosine-triphosphate-cyclohydrolase-1 (GTP-CH1) pathway. Furthermore, markers of the two pathways appeared to correlate with divergent depressive symptoms. The commentary points out however, that few of the subjects met criteria for a major depressive episode.

Commentary by John C.S. Breitner

Schneider P, Buerger K, Teipel S, et al (2011). Antihypertensive therapy is associated with reduced rate of conversion to Alzheimer's disease in midregional proatrial natriuretic peptide stratified subjects with mild cognitive impairment. Biol Psychiatry 70:145-151

Several lines of evidence suggest that hypertension and vasculopathy represent significant risk factors for Alzheimer's disease (AD). In this paper Dr. Schneider and colleagues examined the relationship between conversion from mild cognitive impairment (MCI) to AD and midregional proatrial natriuretic peptide (MR-proANP). MR-proANP is a surrogate for atrial natriuretic peptide (ANP), a molecule involved in the regulation of blood pressure. The authors found that baseline MR-proANP was significantly increased in individuals who converted to AD. However, treatment with antihypertensive medication significantly decreased conversion to AD only in those individuals with baseline elevation of MR-proANP, suggesting that treatment of elevated blood pressure may be helpful in preventing progression to AD only in these patients.


August 1, 2011 


Commentary by Michael W. Otto

Modi ME, Young LJ (2011). D-cycloserine facilitates socially reinforced learning in an animal model relevant to autism spectrum disorders. Biol Psychiatry 70:298-304

In this study the authors build on previous findings that the NMDA receptor partial agonist, d-cycloserine (DCS), may enhance extinction learning and provide a useful adjunct to psychotherapeutic interventions for a variety of anxiety disorders. The authors apply DCS to modify the formation of partner preference in prairie voles. A low dose of peripheral DCS or microinjection of DCS to the amygdala or nucleus accumbens was associated with more rapid preference formation. The authors suggest that this effect is mediated through oxytocin-mediated social learning systems, and further suggest that DCS may be useful for treating the social impairment associated with autism spectrum disorders (ASD). While noting the importance of this study, the commentary provides some alternate explanations for the study findings.

Commentary by Risto Näätänen and Teija Kujala

Roberts TP, Cannon KM, Tavabi K, et al (2011). Auditory magnetic mismatch field latency: a biomarker for language impairment in autism. Biol Psychiatry 70:263-269

Magnetic mismatch field latency (MMF) has previously been shown to be affected by autism spectrum disorders (ASD), and may be associated with clinical language impairment. In this study, the authors found evidence for prolonged MMF latency in children with ASD; delay was greatest in children with language impairments. The authors suggest that MMF may help provide a neurobiological marker for language impairments and serve as a potential biomarker for deficits in language development. The commentary elaborates on the authors' speculation as to how specific these findings might be to language development in ASD, and suggest that an association between MMF findings and a more general cognitive decline cannot be ruled out.

Commentary by Ahmad R. Hariri

Salatino-Oliveira A, Genro JP, Zeni C, et al (2011). Catechol-O-methyltransferase valine158methionine polymorphism moderates methylphenidate effects on oppositional symptoms in boys with attention-deficit/hyperactivity disorder. Biol Psychiatry 70:216-221

The effects of the substitution of valine for methionine at codon 158 (val158met) on the function of the catechol-O-methyltransferase enzyme (COMT) have been well documented over the more than ten years since it was first linked to psychiatric symptomatology. In this paper, Salatino-Oliveira and colleagues report that the val158met polymorphism is associated with the effects of methylphenidate treatment in children with attention deficit hyperactivity disorder (ADHD). The commentary places these findings in the larger context of COMT studies and notes that these findings suggest the importance of developmental stage in the manifestation of val158met effects.

Dumontheil I, Roggeman C, Ziermans T, et al (2011). Influence of the COMT genotype on working memory and brain activity changes during development. Biol Psychiatry 70:222-229

The met allele of the val158met COMT polymorphism has been associated with decreased prefrontal activation and improved performance on working memory tasks in adults. In this study, the authors report that this improvement does not appear until after 10 years of age. They also note an age by genotype interaction with regard to functional activation and gray matter volume in some brain regions. The commentary juxtaposes these findings with those of Salatino-Oliveira and colleagues in demonstrating disparate developmental influences on the effects of this polymorphism.


August 15, 2011 


Commentary by Mark D. Underwood and Victoria Arango

Ernst C, Nagy C, Kim S, et al (2011). Dysfunction of astrocyte connexins 30 and 43 in dorsal lateral prefrontal cortex of suicide completers. Biol Psychiatry 70:312-319

There is increasing evidence that suicide may comprise a distinct phenotype separate or in addition to underlying psychiatric disorders. In this study Dr. Ernst and colleagues report that they found astrocyte connexins 30 and 40 to be down regulated in the dorsolateral prefrontal cortex (DLPFC) of suicide completers. The authors suggest that connexins may be related to mood symptoms and antidepressant response. In the commentary it is further suggested that these findings may have broader implications, including questions around the role of astrocytes in psychiatric disorders and the potential developmental nature of vulnerability to suicide.

Cyprien F, Courtet P, Malafosse A, et al (2011). Suicidal behavior is associated with reduced corpus callosum area. Biol Psychiatry 70:320-326

The authors found reductions in the caudal third of the corpus callosum (CC) in older adults who had attempted suicide- even versus a group of affective controls. The commentary notes that these findings are in contrast to previous studies that have found changes in the anterior portion of the CC, which encompasses the majority of prefrontal interconnections. They speculate that these differences might be related to the older age of the subjects here, or their having failed to complete suicide; the latter presumably representing evidence of resilience. Taken together with the above study, the commentary further suggests that the phenotype of suicide may be related to multiple neurobiological substrates.

Commentary by Yvette I. Sheline

Gerritsen L, Comijs HC, van der Graaf Y, et al (2011). Depression, hypothalamic pituitary adrenal axis, and hippocampal and entorhinal cortex volumes--the SMART Medea study. Biol Psychiatry 70:373-380

In this large study of participants from the second Manifestation of ARTerial disease-Memory depression and aging (SMART-Medea) study, the authors observed smaller hippocampal volumes in patients with a history of depression and in patients with early-onset depression. Remitted major depressive disorder was associated with smaller entorhinal volumes. Of particular interest were findings in patients with late-onset depression, first diagnosed at 50 years-of-age or older. The authors observed decreased entorhinal volumes in these patients, but they did not demonstrate reduced hippocampal volume. Although the authors did not observe evidence of any association with measures of hypothalamic-pituitary-adrenal (HPA) axis regulation, patients were not acutely depressed when these were obtained. The commentary places these findings in a larger context, as well as noting that the decreased entorhinal volume in late-onset patients might be related to early dementia-related changes rather than depression. The commentary further argues the need for prospective studies, and studies of the HPA during acute depressive episodes to better address issues with neurobiological causality in depression.

Commentary by Marc G. Berman and John Jonides

Hamilton JP, Furman DJ, Chang C, et al (2011). Default-mode and task-positive network activity in major depressive disorder: implications for adaptive and maladaptive rumination. Biol Psychiatry 70:327-333

The authors compared activity in the default-mode network (DMN) versus the task-positive network (TPN) in a group of depressed adults. Individuals with depression significantly differed from healthy controls; furthermore, increased activity in the DMN was associated with more depressive rumination and lower levels of more adaptive, reflective rumination. Activation of the right fronto-insular cortex (RFIC) an area hypothesized to be involved in switching between DMN and TPN dominance, at the onset of DMN activity was reversed in depressed individuals versus healthy controls. The commentary expands on these findings and places them in a larger context.


September 1, 2011 


Commentary by Rachel Yehuda

Dietz DM, Laplant Q, Watts EL, et al (2011). Paternal transmission of stress-induced pathologies. Biol Psychiatry 70:408-414

The transmission to offspring of the effects of maternal stress has generally been assumed to be rooted in the influence of the uterine environmental or to be transmitted through stress-related behavioral change in the mother. In this study the authors study the effects of paternal stress on male and female offspring. Dr. Dietz and colleagues report that exposure to chronic social defeat is associated with increased measures of depression- and anxiety-like behaviors in the offspring of adult male mice. Only male offspring however, showed concomitant hormonal changes. These findings were present only in offspring produced through copulation, and was not seen in offspring that resulted from in vitro fertilization. The authors suggest that this discrepancy is indicative of influences from the copulatory behavior rather than epigenetic changes in the fathers. These findings are discussed in the commentary, and the point is made that the discrepant IVF findings might be related to technical issues rather than ruling out potential epigenetic changes.

Commentary by Hymie Anisman

Olson VG, Rockett HR, Reh RK, et al (2011). The role of norepinephrine in differential response to stress in an animal model of posttraumatic stress disorder. Biol Psychiatry 70:441-448

The authors utilize a sophisticated rodent model of posttraumatic stress disorder (PTSD) to study the effects of a single prolonged stress followed by repeated behavioral cues on behavioral change and brain activation during a force swim test- reflected in c-fos expression. Exposed rodents were divided into susceptible and resistant groups based on their response to the stressor. Susceptible mice showed aggressive and social behavioral correlates of PTSD that were normalized with pharmacologic manipulation of norepinephrine pathways, activation of inhibitory autoreceptors or blockade of postsynaptic α1-adrenoreceptors. In the commentary, Dr. Anisman places these findings in the context of recent PTSD research and suggests that the different phases of the illness might be associated with distinct neurobiological processes.

Commentary by Laura M. Rowland

Delgado y Palacios R, Campo A, Henningsen K, et al (2011). Magnetic resonance imaging and spectroscopy reveal differential hippocampal changes in anhedonic and resilient subtypes of the chronic mild stress rat model. Biol Psychiatry 70:449-457

 In this paper, the authors examine the results of chronic mild stress (CMS) in a group of twelve week-old rats. After the CMS, rats were divided by response into resilient and anhedonic categories based on sucrose intake. Both resilient and anhedonic rats showed hippocampal diffusion and histological changes, compared with a group of control rats. Susceptible rats differed from their resilient counterparts however, on some morphological features of the hippocampus and magnetic resonance spectroscopy measures of glutamate/creatine and N-acetylaspartylglutamate (NAAG)/creatine ratios. The authors note that their findings emphasize the potential role played by hippocampal pathology in depression and suggest that stress-induced hippocampal reorganization differs between resilient and susceptible rats. While some weaknesses in the study design are discussed in the commentary, findings are placed in a clinical context and used to illustrate the promise of multi-modal imaging.


September 15, 2011 


Commentary by Howard J. Edenberg

Heath AC, Whitfield JB, Martin NG, et al (2011). A quantitative-trait genome-wide association study of alcoholism risk in the community: findings and implications. Biol Psychiatry 70:513-518

The authors have performed a genome-wide single nucleotide polymorphism (SNP) genotyping with a large group of sibships. They performed family-based association tests for measures of alcohol abuse and dependence, as well as consumption. Dr. Heath and colleagues did not report any findings achieving genome-wide significance but note data suggesting roles for two genes and a number of SNPs with small effect sizes. They conclude that applying GWAS results clinically may be difficult. The commentary discusses the use of this technique in studying alcohol use disorders and notes that it may show more clinical promise than credited by the authors.

Commentary by Kent E. Hutchinson and Lara A. Ray

Xie P, Kranzler HR, Krauthammer M, et al (2011). Rare nonsynonymous variants in alpha-4 nicotinic acetylcholine receptor gene protect against nicotine dependence. Biol Psychiatry 70:528-536

 Previous studies have suggested an association between alpha-4 nicotinic receptors coded by CHRNA4, and nicotine dependence (ND). In this paper, the authors report on their sequencing of coding exons and flanking intronic regions of CHRNA4 in patients with ND and controls- with a larger analysis of exon 5. A protective effect of rare nonsynonymous variants was suggested by the higher frequency in control subjects. Exploratory SPECT scans suggest that some of these variants may be associated with differences in receptor binding.  The commentary places these findings into a larger context and notes that this paper demonstrates both the role that rare variants may play in ND and the potential power of cross-modality studies for generating new neurophysiologic insights.

Commentary by Mary Jeanne Kreek, Yan Zhou, and Orna Levran

Maher BS, Vladimirov VI, Latendresse SJ, et al (2011). The AVPR1A Gene and Substance Use Disorders: Association, Replication, and Functional Evidence. Biol Psychiatry 70:519-527

The authors report their findings of an association between three single nucleotide polymorphisms (SNPs) and substance use disorder (SUD). These SNPs were in the arginine vasopressin (AVP) 1A receptor gene, AVPR1A which has been associated with social behavior and emotional arousal. The effects of one of these SNPs on SUD was found to be mediated by spousal satisfaction. This genotype was also found to impact AVPR1A expression in a collection of postmortem brain samples. While the associate with SUD was not replicated in a population-based sample, the authors suggest that the relatively lower severity of use in these subjects may be germane. In the commentary, these AVP findings are placed in the context of the commentators' previous work.


October 1, 2011 


Commentary by Daniel H. Mathalon

Wood SJ, Yung AR, McGorry PD, et al (2011). Neuroimaging and treatment evidence for clinical staging in psychotic disorders: from the at-risk mental state to chronic schizophrenia. Biol Psychiatry 70:619-625

In this paper, Wood and colleagues apply a proposed staging model of psychiatric disorders to schizophrenia. The authors propose defined stages from 0 through IV (with I divided into Ia and Ib). They review both imaging and clinical data supporting the use of staging in schizophrenia. The commentary reviews the proposed use of staging in psychiatry but notes that the data cited by Wood and colleagues could equally support a continuum-based model of schizophrenia, and the lack of clear therapeutic application of these stages. Nonetheless, the commentary notes that the approach holds potential promise.  

Commentary by Margaret A. Cooper and Anthony J. Koleske

Neddens J, Fish KN, Tricoire L, et al (2011). Conserved Interneuron-Specific ErbB4 Expression in Frontal Cortex of Rodents, Monkeys, and Humans: Implications for Schizophrenia. Biol Psychiatry 70:636-645

The neuroregulin-1 ErbB4 signaling pathway has been widely implicated in the pathophysiology of schizophrenia. Localization of ErbB4 in primates however, has remained controversial. In this paper, the authors examined ErbB4 expression across rodent, non-human primate, and human subjects. No presynaptic expression was observed, and predominate localization to interneurons was conserved across species. The commentary discusses these findings in depth and notes that this study is particularly important in validating the use of rodent models to study the possible role of ErbB4 in schizophrenia.

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


2011 Annual Meeting - Plenary Speaker Recordings
Did you miss the 2011 annual meeting in San Francisco, or did you attend but want to listen to one of the plenary speakers again?  For the 2011 meeting, we've made available a link for your use.  We will consider recording these sessions at future meetings but we need to know if this is a benefit you would like to receive.   Send your feedback to sobp@sobp.org, and enjoy the talks.

2011 Annual Meeting Plenary Talks
Membership Renewals for 2012
2012 Membership Renewals due December 31, 2011

Stay connected and engaged - Renew your membership for 2012 now
and continue to receive your member benefits:    
  1. Subscription to our top-rated journal, Biological Psychiatry
  2. Reduced registration fees for the annual meeting
  3. Reduced abstract submission fees for the annual meeting 
  4. Sponsor abstracts and membership applications
  5. Access to members-only on-line tools
  6. Leadership opportunities on committees or as officers of the Society 
  7. Recognition and affiliation with a premier organization
  8. Networking and professional development
Renew on-line at www.sobp.org.  If you need your login information or an invoice for payment email sobp@sobp.org 

Renewal invoices for 2012 will be emailed to you October 1, 2011  If you do not receive or have questions, please let us know.  sobp@sobp.org
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William B. Lawson, MD, PhD
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