News and Commentary Archive

Explore recent scientific discoveries and news as well as CLBB events, commentary, and press.


The speed of technology in neuroscience as it impacts ethical and just decisions in the legal system needs to be understood by lawyers, judges, public policy makers, and the general public. The Massachusetts General Hospital Center for Law, Brain, and Behavior is an academic and professional resource for the education, research, and understanding of neuroscience and the law. Read more

Does Developmental Timing of Exposure to Child Maltreatment Predict Memory Performance in Adulthood? Results from a Large, Population-Based Sample

By Erin C. Dunn, Daniel S. Busso, Miriam R. Raffeld, Jordan W. Smoller, Charles A. Nelson, Alysa E. Doyle, and Gigi Luk | Child Abuse & Neglect | November 13, 2015


Although maltreatment is a known risk factor for multiple adverse outcomes across the lifespan, its effects on cognitive development, especially memory, are poorly understood. Using data from a large, nationally representative sample of young adults (Add Health), we examined the effects of physical and sexual abuse on working and short-term memory in adulthood. We examined the association between exposure to maltreatment as well as its timing of first onset after adjusting for covariates. Of our sample, 16.50% of respondents were exposed to physical abuse and 4.36% to sexual abuse by age 17. An analysis comparing unexposed respondents to those exposed to physical or sexual abuse did not yield any significant differences in adult memory performance. However, two developmental time periods emerged as important for shaping memory following exposure to sexual abuse, but in opposite ways. Relative to non-exposed respondents, those exposed to sexual abuse during early childhood (ages 3-5), had better number recall and those first exposed during adolescence (ages 14-17) had worse number recall. However, other variables, including socioeconomic status, played a larger role (than maltreatment) on working and short-term memory. We conclude that a simple examination of “exposed” versus “unexposed” respondents may obscure potentially important within-group differences that are revealed by examining the effects of age at onset to maltreatment.

Read the entire paper here.

Genome-Wide Association Study Identifies SESTD1 as a Novel Risk Gene for Lithium-Responsive Bipolar Disorder

By J. Song, Sarah E. Bergen, Arianna Di Florio, R. Karlsson, Alexander Charney, Douglas M. Ruderfer, Eli A. Stahl, Members of the International Cohort Collection for Bipolar Disorder (ICCBD), Kimberly D. Chambert, Jennifer L. Moran, Katherine Gordon-Smith, Liz Forty, Elaine K. Green, Ian Jones, Lisa Jones, E. M. Scolnick, Pamela Sklar, Jordan W. Smoller, P. Lichtenstein, Christina Hultman, Nick Craddock, and Mikael Landén | Molecular Psychiatry | October 27, 2015


Lithium is the mainstay prophylactic treatment for bipolar disorder (BD), but treatment response varies considerably across individuals. Patients who respond well to lithium treatment might represent a relatively homogeneous subtype of this genetically and phenotypically diverse disorder. Here, we performed genome-wide association studies (GWAS) to identify (i) specific genetic variations influencing lithium response and (ii) genetic variants associated with risk for lithium-responsive BD. Patients with BD and controls were recruited from Sweden and the United Kingdom. GWAS were performed on 2698 patients with subjectively defined (self-reported) lithium response and 1176 patients with objectively defined (clinically documented) lithium response. We next conducted GWAS comparing lithium responders with healthy controls (1639 subjective responders and 8899 controls; 323 objective responders and 6684 controls). Meta-analyses of Swedish and UK results revealed no significant associations with lithium response within the bipolar subjects. However, when comparing lithium-responsive patients with controls, two imputed markers attained genome-wide significant associations, among which one was validated in confirmatory genotyping (rs116323614, P=2.74 × 10−8). It is an intronic single-nucleotide polymorphism (SNP) on chromosome 2q31.2 in the gene SEC14 and spectrin domains 1 (SESTD1), which encodes a protein involved in regulation of phospholipids. Phospholipids have been strongly implicated as lithium treatment targets. Furthermore, we estimated the proportion of variance for lithium-responsive BD explained by common variants (‘SNP heritability’) as 0.25 and 0.29 using two definitions of lithium response. Our results revealed a genetic variant in SESTD1 associated with risk for lithium-responsive BD, suggesting that the understanding of BD etiology could be furthered by focusing on this subtype of BD.

Read the full paper here.

Nicotine Dependence and Psychosis in Bipolar Disorder and Schizoaffective Disorder, Bipolar Type

By Elena Estrada, Sarah M. Hartz, Jeffrey Tran, Donald M. Hilty, Pamela Sklar, Jordan W. Smoller, Carlos N. Pato, Michele T. Pato, and Genomic Psychiatry Cohort Consortium | American Journal of Medical Genetics | October 15, 2015


Patients with Bipolar disorder smoke more than the general population. Smoking negatively impacts mortality and clinical course in Bipolar disorder patients. Prior studies have shown contradictory results regarding the impact of psychosis on smoking behavior in Bipolar disorder. We analyzed a large sample of Bipolar disorder and Schizoaffective disorder, Bipolar Type patients and predicted those with a history of psychosis would be more likely to be nicotine dependent. Data from subjects and controls were collected from the Genomic Psychiatry Cohort (GPC). Subjects were diagnosed with Bipolar disorder without psychosis (N = 610), Bipolar disorder with psychosis (N = 1544). Participants were classified with or without nicotine dependence. Diagnostic groups were compared to controls (N = 10065) using logistic regression. Among smokers (N = 6157), those with Bipolar disorder had an increased risk of nicotine dependence (OR = 2.5; P < 0.0001). Patients with Bipolar disorder with psychosis were more likely to be dependent than Bipolar disorder patients without psychosis (OR = 1.3; P = 0.03). Schizoaffective disorder, Bipolar Type patients had more risk of nicotine dependence when compared to Bipolar disorder patients with or without psychosis (OR = 1.2; P = 0.02). Bipolar disorder patients experiencing more severity of psychosis have more risk of nicotine dependence.

Read the full paper here.

Individual Aesthetic Preferences for Faces Are Shaped Mostly by Environments, Not Genes

By Laura Germine, Richard Russell, P. Matthew Bronstad, Gabriëlla A.M. Blokland, Jordan W. Smoller, Holum Kwok, Samuel E. Anthony, Ken Nakayama, Gillian Rhodes, and Jeremy B. Wilmer | Current Biology | October 1, 2015


Although certain characteristics of human faces are broadly considered more attractive (e.g., symmetry, averageness), people also routinely disagree with each other on the relative attractiveness of faces. That is, to some significant degree, beauty is in the “eye of the beholder.” Here, we investigate the origins of these individual differences in face preferences using a twin design, allowing us to estimate the relative contributions of genetic and environmental variation to individual face attractiveness judgments or face preferences. We first show that individual face preferences (IP) can be reliably measured and are readily dissociable from other types of attractiveness judgments (e.g., judgments of scenes, objects). Next, we show that individual face preferences result primarily from environments that are unique to each individual. This is in striking contrast to individual differences in face identity recognition, which result primarily from variations in genes [1]. We thus complete an etiological double dissociation between two core domains of social perception (judgments of identity versus attractiveness) within the same visual stimulus (the face). At the same time, we provide an example, rare in behavioral genetics, of a reliably and objectively measured behavioral characteristic where variations are shaped mostly by the environment. The large impact of experience on individual face preferences provides a novel window into the evolution and architecture of the social brain, while lending new empirical support to the long-standing claim that environments shape individual notions of what is attractive.

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Extending the ‘Cross-Disorder’ Relevance of Executive Functions to Dimensional Neuropsychiatric Traits in Youth

By Lauren M. McGrath, Ellen B. Braaten, Nathan D. Doty, Brian L. Willoughby, H. Kent Wilson, Ellen H. O’Donnell, Mary K. Colvin, Hillary L. Ditmars, Jessica E. Blais, Erin N. Hill, Aaron Metzger, Roy H. Perlis, Erik G. Willcutt, Jordan W. Smoller, Irwin D. Waldman, Stephen V. Faraone, Larry J. Seidman, and Alysa E. Doyle | The Journal of Child Psychology and Psychiatry | September 28, 2015



Evidence that different neuropsychiatric conditions share genetic liability has increased interest in phenotypes with ‘cross-disorder’ relevance, as they may contribute to revised models of psychopathology. Cognition is a promising construct for study; yet, evidence that the same cognitive functions are impaired across different forms of psychopathology comes primarily from separate studies of individual categorical diagnoses versus controls. Given growing support for dimensional models that cut across traditional diagnostic boundaries, we aimed to determine, within a single cohort, whether performance on measures of executive functions (EFs) predicted dimensions of different psychopathological conditions known to share genetic liability.


Data are from 393 participants, ages 8–17, consecutively enrolled in the Longitudinal Study of Genetic Influences on Cognition (LOGIC). This project is conducting deep phenotyping and genomic analyses in youth referred for neuropsychiatric evaluation. Using structural equation modeling, we examined whether EFs predicted variation in core dimensions of the autism spectrum disorder, bipolar illness, and schizophrenia (including social responsiveness, mania/emotion regulation, and positive symptoms of psychosis, respectively).


We modeled three cognitive factors (working memory, shifting, and executive processing speed) that loaded on a second-order EF factor. The EF factor predicted variation in our three target traits, but not in a negative control (somatization). Moreover, this EF factor was primarily associated with the overlapping (rather than unique) variance across the three outcome measures, suggesting that it related to a general increase in psychopathology symptoms across those dimensions.


Findings extend support for the relevance of cognition to neuropsychiatric conditions that share underlying genetic risk. They suggest that higher-order cognition, including EFs, relates to the dimensional spectrum of each of these disorders and not just the clinical diagnoses. Moreover, results have implications for bottom-up models linking genes, cognition, and a general psychopathology liability.

Read the full article here.