Person: Faraone, Stephen
Loading...
Email Address
AA Acceptance Date
Birth Date
Research Projects
Organizational Units
Job Title
Last Name
Faraone
First Name
Stephen
Name
Faraone, Stephen
12 results
Search Results
Now showing 1 - 10 of 12
Publication Identifying Pediatric Mood Disorders From Transdiagnostic Polygenic Risk Scores: A Study of Children and Adolescents(Physicians Postgraduate Press, Inc, 2022-04-20) Barnett, Eric J.; Biederman, Joseph; Doyle, Alysa; Hess, Jonathan; DiSalvo, Maura; Faraone, StephenPublication Further evidence of low adherence to stimulant treatment in adult ADHD: an electronic medical record study examining timely renewal of a stimulant prescription(Springer Science and Business Media LLC, 2020-06-26) Biederman, Joseph; Fried, Ronna; DiSalvo, Maura; Biederman, Itai; Woodworth, K. Yvonne; Noyes, Elizabeth; Driscoll, Haley; Faraone, Stephen; Perlis, RoyPublication High Loading of Polygenic Risk for ADHD in Children With Comorbid Aggression(American Psychiatric Association, 2014) Hamshere, Marian L.; Langley, Kate; Martin, Joanna; Agha, Sharifah Shameem; Stergiakouli, Evangelia; Anney, Richard J.L.; Buitelaar, Jan; Faraone, Stephen; Lesch, Klaus-Peter; Neale, Benjamin; Franke, Barbara; Sonuga-Barke, Edmund; Asherson, Philip; Merwood, Andrew; Kuntsi, Jonna; Medland, Sarah E.; Ripke, Stephan; Steinhausen, Hans-Christoph; Freitag, Christine; Reif, Andreas; Renner, Tobias J.; Romanos, Marcel; Romanos, Jasmin; Warnke, Andreas; Meyer, Jobst; Palmason, Haukur; Vasquez, Alejandro Arias; Lambregts-Rommelse, Nanda; Roeyers, Herbert; Biederman, Joseph; Doyle, Alysa; Hakonarson, Hakon; Rothenberger, Aribert; Banaschewski, Tobias; Oades, Robert D.; McGough, James J.; Kent, Lindsey; Williams, Nigel; Owen, Michael J.; Holmans, Peter; O’Donovan, Michael C.; Thapar, AnitaObjective: Although attention deficit hyperactivity disorder (ADHD) is highly heritable, genome-wide association studies (GWAS) have not yet identified any common genetic variants that contribute to risk. There is evidence that aggression or conduct disorder in children with ADHD indexes higher genetic loading and clinical severity. The authors examine whether common genetic variants considered en masse as polygenic scores for ADHD are especially enriched in children with comorbid conduct disorder. Method Polygenic scores derived from an ADHD GWAS meta-analysis were calculated in an independent ADHD sample (452 case subjects, 5,081 comparison subjects). Multivariate logistic regression analyses were employed to compare polygenic scores in the ADHD and comparison groups and test for higher scores in ADHD case subjects with comorbid conduct disorder relative to comparison subjects and relative to those without comorbid conduct disorder. Association with symptom scores was tested using linear regression. Results: Polygenic risk for ADHD, derived from the meta-analysis, was higher in the independent ADHD group than in the comparison group. Polygenic score was significantly higher in ADHD case subjects with conduct disorder relative to ADHD case subjects without conduct disorder. ADHD polygenic score showed significant association with comorbid conduct disorder symptoms. This relationship was explained by the aggression items. Conclusions: Common genetic variation is relevant to ADHD, especially in individuals with comorbid aggression. The findings suggest that the previously published ADHD GWAS meta-analysis contains weak but true associations with common variants, support for which falls below genome-wide significance levels. The findings also highlight the fact that aggression in ADHD indexes genetic as well as clinical severity.Publication Hyperactivity and hyperconnectivity of the default network in schizophrenia and in first-degree relatives of persons with schizophrenia(Proceedings of the National Academy of Sciences, 2009) Whitfield-Gabrieli, S.; Thermenos, Heidi; Milanovic, Snezana M.; Tsuang, Ming; Faraone, Stephen; McCarley, Robert William; Shenton, Martha; Green, Alan; Nieto-Castanon, A.; LaViolette, P.; Wojcik, Joanne; Gabrieli, John; Seidman, Larry JoelWe examined the status of the neural network mediating the default mode of brain function, which typically exhibits greater activation during rest than during task, in patients in the early phase of schizophrenia and in young first-degree relatives of persons with schizophrenia. During functional MRI, patients, relatives, and controls alternated between rest and performance of working memory (WM) tasks. As expected, controls exhibited task-related suppression of activation in the default network, including medial prefrontal cortex (MPFC) and posterior cingulate cortex/precuneus. Patients and relatives exhibited significantly reduced task-related suppression in MPFC, and these reductions remained after controlling for performance. Increased task-related MPFC suppression correlated with better WM performance in patients and relatives and with less psychopathology in all 3 groups. For WM task performance, patients and relatives had greater activation in right dorsolateral prefrontal cortex (DLPFC) than controls. During rest and task, patients and relatives exhibited abnormally high functional connectivity within the default network. The magnitudes of default network connectivity during rest and task correlated with psychopathology in the patients. Further, during both rest and task, patients exhibited reduced anticorrelations between MPFC and DLPFC, a region that was hyperactivated by patients and relatives during WM performance. Among patients, the magnitude of MPFC task suppression negatively correlated with default connectivity, suggesting an association between the hyperactivation and hyperconnectivity in schizophrenia. Hyperactivation (reduced task-related suppression) of default regions and hyperconnectivity of the default network may contribute to disturbances of thought in schizophrenia and risk for the illness.Publication Does the Mixed Opioid Receptor Antagonist Naltrexone Mitigate Stimulant-Induced Euphoria?: A Double-Blind, Placebo Controlled Trial of NaltrexoneSpencer, Thomas; Bhide, Pradeep; Zhu, Jinmin; Faraone, Stephen; Fitzgerald, Maura; Yule, Amy; Uchida, Mai; Spencer, Andrea; Hall, Anna M.; Koster, Ariana J.; Feinberg, Leah; Kassabian, Sarah; Storch, Barbara; Biederman, JosephPublication Longitudinal Course of Deficient Emotional Self-Regulation CBCL Profile in Youth with ADHD: Prospective Controlled Study(Dove Medical Press, 2012) Biederman, Joseph; Spencer, Thomas; Petty, Carter; Hyder, Laran L; O’Connor, Katherine B; Surman, Craig; Faraone, StephenBackground: While symptoms of deficient emotional self-regulation (DESR) have been long associated with attention-deficit/hyperactivity disorder (ADHD), there has been limited investigation of this aspect of the clinical picture of the disorder. The main aim of this study was to examine the predictive utility of DESR in moderating the course of ADHD children into adolescence. Methods: Subjects comprised 177 children with and 204 children without ADHD followed for an average of 4 years (aged 6–18 years at baseline, 54% male). Subjects were assessed with structured diagnostic interviews and measures of psychosocial functioning. DESR was defined by the presence (n = 79) or absence (n = 98) of Child Behavior Checklist (CBCL)-DESR profile (score ≥ 180 < 210 total of Attention, Aggression, and Anxious/Depressed subscales) at the baseline assessment. Results: Of subjects with DESR at baseline, 57% had DESR at follow-up. Persistent ADHD was significantly associated with DESR at follow-up (x\(^{2}\)\(_{(1)}\) = 15.37, P < 0.001). At follow-up, ADHD + DESR subjects had significantly more comorbidities (z = 2.55, P = 0.01), a higher prevalence of oppositional defiant disorder (z = 3.01, P = 0.003), and more impaired CBCL social problems t-score (t\(_{(227)}\) = 2.41, P = 0.02) versus ADHD subjects. Conclusion: This work suggests that a positive CBCL-DESR profile predicts subsequent psychopathology and functional impairments in children with ADHD suggesting that it has the potential to help identify children with ADHD at high risk for compromised outcomes.Publication Genome-Wide Analysis of Copy Number Variants in Attention Deficit Hyperactivity Disorder: The Role of Rare Variants and Duplications at 15q13.3(American Psychiatric Publishing, 2013) Williams, Nigel M.; Franke, Barbara; Mick, Eric; Anney, Richard J.L.; Freitag, Christine M.; Gill, Michael; Thapar, Anita; O'Donovan, Michael C.; Owen, Michael J.; Holmans, Peter; Kent, Lindsey; Middleton, Frank; Zhang-James, Yanli; Liu, Lu; Meyer, Jobst; Nguyen, Thuy Trang; Romanos, Jasmin; Romanos, Marcel; Seitz, Christiane; Renner, Tobias J.; Walitza, Susanne; Warnke, Andreas; Palmason, Haukur; Buitelaar, Jan; Rommelse, Nanda; Vasquez, Alejandro Arias; Hawi, Ziarih; Langley, Kate; Sergeant, Joseph; Steinhausen, Hans-Christoph; Roeyers, Herbert; Biederman, Joseph; Zaharieva, Irina; Hakonarson, Hakon; Elia, Josephine; Lionel, Anath C.; Crosbie, Jennifer; Marshall, Christian R.; Schachar, Russell; Scherer, Stephen W.; Todorov, Alexandre; Smalley, Susan L.; Loo, Sandra; Nelson, Stanley; Shtir, Corina; Asherson, Philip; Reif, Andreas; Lesch, Klaus-Peter; Faraone, StephenObjective: Attention deficit hyperactivity disorder (ADHD) is a common, highly heritable psychiatric disorder. Because of its multifactorial etiology, however, identifying the genes involved has been difficult. The authors followed up on recent findings suggesting that rare copy number variants (CNVs) may be important for ADHD etiology. Method: The authors performed a genome-wide analysis of large, rare CNVs (<1% population frequency) in children with ADHD (N=896) and comparison subjects (N=2,455) from the IMAGE II Consortium. Results: The authors observed 1,562 individually rare CNVs >100 kb in size, which segregated into 912 independent loci. Overall, the rate of rare CNVs >100 kb was 1.15 times higher in ADHD case subjects relative to comparison subjects, with duplications spanning known genes showing a 1.2-fold enrichment. In accordance with a previous study, rare CNVs >500 kb showed the greatest enrichment (1.28-fold). CNVs identified in ADHD case subjects were significantly enriched for loci implicated in autism and in schizophrenia. Duplications spanning the CHRNA7 gene at chromosome 15q13.3 were associated with ADHD in single-locus analysis. This finding was consistently replicated in an additional 2,242 ADHD case subjects and 8,552 comparison subjects from four independent cohorts from the United Kingdom, the United States, and Canada. Presence of the duplication at 15q13.3 appeared to be associated with comorbid conduct disorder. Conclusions: These findings support the enrichment of large, rare CNVs in ADHD and implicate duplications at 15q13.3 as a novel risk factor for ADHD. With a frequency of 0.6% in the populations investigated and a relatively large effect size (odds ratio=2.22, 95% confidence interval=1.5–3.6), this locus could be an important contributor to ADHD etiology.Publication Discriminant and Concurrent Validity of a Simplified DSM-Based Structured Diagnostic Instrument for the Assessment of Autism Spectrum Disorders in Youth and Young Adults(BioMed Central, 2011) Petty, Carter R; Galdo, Maribel; Kotarski, Meghan; Caruso, Janet; Meller, Benjamin; Joshi, Gagan; Fried, Ronna; Wozniak, Janet; Micco, Jamie; Henin, Aude; Doyle, Robert; Faraone, Stephen; Biederman, JosephBackground: To evaluate the concurrent and discriminant validity of a brief DSM-based structured diagnostic interview for referred individuals with autism spectrum disorders (ASDs). Methods: To test concurrent validity, we assessed the structured interview's agreement in 123 youth with the expert clinician assessment and the Social Responsiveness Scale (SRS). Discriminant validity was examined using 1563 clinic-referred youth. Results: The structured diagnostic interview and SRS were highly sensitive indicators of the expert clinician assessment. Equally strong was the agreement between the structured interview and SRS. We found evidence for high specificity for the structured interview. Conclusions: A simplified DSM-based ASD structured diagnostic interview could serve as a useful diagnostic aid in the assessment of subjects with ASDs in clinical and research settings.Publication A Laboratory Driving Simulation for Assessment of Driving Behavior in Adults with ADHD: A Controlled Study(BioMed Central, 2007) Monuteaux, Michael C; Reimer, Bryan; Coughlin, Joseph F; Aleardi, Megan; Dougherty, Meghan; Schoenfeld, Steven; Biederman, Joseph; Fried, Ronna; Surman, Craig; Spencer, Thomas; Faraone, StephenBackground: It is now estimated that attention deficit-hyperactivity disorder (ADHD) afflicts at least 4% of adults in the United States and is associated with high levels of morbidity and functional impairment. One key area of dysfunction associated with ADHD is impaired motor vehicle operation. Our goal was to examine the association between ADHD and specific driving outcomes in a sample of adults using a driving simulator. Methods: Subjects were 20 adults with full DSM-IV ADHD and 21 controls without ADHD of equal gender distribution. However, the mean age of subjects with ADHD was somewhat older. All analyses were adjusted for age and gender. All subjects participated in a driving simulation that lasted for one hour and consisted of a short training period, a high stimulus segment and a low stimulus segment with two distinct monotonous periods. Results: In the second monotonous period within the low stimulus environment, ADHD subjects were significantly more likely than controls to collide with an obstacle suddenly appearing from the periphery, adjusting for age and gender. Conclusion: Adults with ADHD were more likely than controls to collide with an obstacle during a driving simulation suggesting that deficits in directed attention may underlie driving impairments in this population.Publication Family-based association study of the BDNF, COMT and serotonin transporter genes and DSM-IV bipolar-I disorder in children(BioMed Central, 2009) Mick, Eric Owen; Wozniak, Janet; Wilens, Timothy; Biederman, Joseph; Faraone, StephenBackground: Over the past decade pediatric bipolar disorder has gained recognition as a potentially more severe and heritable form of the disorder. In this report we test for association with genes coding brain-derived neurotrophic factor (BDNF), the serotonin transporter (SLC6A4), and catechol-O-methyltransferase (COMT). Methods: Bipolar-I affected offspring triads (N = 173) were drawn from 522 individuals with 2 parents in 332 nuclear families recruited for genetic studies of pediatric psychopathology at the Clinical and Research Program in Pediatric Psychopharmacology and Adult ADHD at Massachusetts General Hospital. Results: We failed to identify an association with the val66 allele in BDNF (OR = 1.23, p = 0.36), the COMT-l allele (OR = 1.27, p = 0.1), or the HTTLPR short allele (OR = 0.87, p = 0.38). Conclusion: Our study suggests that the markers examined thus far in COMT and SLC6A4 are not associated with pediatric bipolar disorder and that if the val66met marker in BDNF is associated with pediatric bipolar disorder the magnitude of the association is much smaller than first reported.