Joachim Hallmayer

Stanford University, Palo Alto, California, United States

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Publications (157)1187.66 Total impact

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    ABSTRACT: Several genetic and environmental factors place youth offspring of parents with bipolar disorder (BD) at high risk for developing mood and anxiety disorders. Recent studies suggest that anxiety symptoms, even at subclinical levels, have been associated with an increased risk for developing BD. The brain-derived neurotrophic factor (BDNF) gene has been implicated in the pathophysiology of both BD and anxiety disorders. We aimed to explore whether anxiety in BD offspring was associated with the BDNF Val66Met polymorphism. 64 BD offspring (mean age: 13.73 (S.D. 3.45) M = 30, F = 34) and 51 HC (mean age: 13.68 (S.D. 2.68) M = 23, F = 28) were compared on presence of the met allele and on scores from the Multidimensional Anxiety Scale for Children (MASC). To assess family function, we used the Family Adaptability and Cohesion Evaluation Scales (FACES-IV). The Baron & Kenny method was the statistical approach used to examine the moderating effects between variables. BD offspring showed higher levels of overall anxiety than did the HC group. BD offspring with the val/val genotype showed higher levels of anxiety than BD offspring with other genotypes. No significant levels of anxiety or its association with BDNF genotype were found in the HC group. BD offspring group showed significantly more family dysfunction when compared with the HC group and the family dysfunction moderated the association between the BDNF genotype and anxiety symptoms. This study demonstrated the potential interplay of three factors: BD offspring, anxiety symptoms and family dysfunction. Copyright © 2014 Elsevier Ltd. All rights reserved.
    Journal of Psychiatric Research 11/2014; · 4.09 Impact Factor
  • Ruth O’Hara, Joachim Hallmayer
    American Journal of Geriatric Psychiatry 10/2014; · 3.52 Impact Factor
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    ABSTRACT: A growing body of research demonstrates that individuals diagnosed with major depressive disorder (MDD) are characterized by shortened telomere length, which has been posited to underlie the association between depression and increased instances of medical illness. The temporal nature of the relation between MDD and shortened telomere length, however, is not clear. Importantly, both MDD and telomere length have been associated independently with high levels of stress, implicating dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and anomalous levels of cortisol secretion in this relation. Despite these associations, no study has assessed telomere length or its relation with HPA-axis activity in individuals at risk for depression, before the onset of disorder. In the present study, we assessed cortisol levels in response to a laboratory stressor and telomere length in 97 healthy young daughters of mothers either with recurrent episodes of depression (i.e., daughters at familial risk for depression) or with no history of psychopathology. We found that daughters of depressed mothers had shorter telomeres than did daughters of never-depressed mothers and, further, that shorter telomeres were associated with greater cortisol reactivity to stress. This study is the first to demonstrate that children at familial risk of developing MDD are characterized by accelerated biological aging, operationalized as shortened telomere length, before they had experienced an onset of depression; this may predispose them to develop not only MDD but also other age-related medical illnesses. It is critical, therefore, that we attempt to identify and distinguish genetic and environmental mechanisms that contribute to telomere shortening.Molecular Psychiatry advance online publication, 30 September 2014; doi:10.1038/mp.2014.119.
    Molecular Psychiatry 09/2014; · 15.15 Impact Factor
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    ABSTRACT: Separate bodies of literature report that elevated pro-inflammatory cytokines and cortisol negatively affect hippocampal structure and cognitive functioning, particularly in older adults. Although interactions between cytokines and cortisol occur through a variety of known mechanisms, few studies consider how their interactions affect brain structure. In this preliminary study, we assess the impact of interactions between circulating levels of IL-1Beta, IL-6, IL-8, IL-10, IL-12, TNF-alpha, and waking cortisol on hippocampal volume. Twenty-eight community-dwelling older adults underwent blood draws for quantification of circulating cytokines and saliva collections to quantify the cortisol awakening response. Hippocampal volume measurements were made using structural magnetic resonance imaging. Elevated levels of waking cortisol in conjunction with higher concentrations of IL-6 and TNF-alpha were associated with smaller hippocampal volumes. In addition, independent of cortisol, higher levels of IL-1beta and TNF-alpha were also associated with smaller hippocampal volumes. These data provide preliminary evidence that higher cortisol, in conjunction with higher IL-6 and TNF-alpha, are associated with smaller hippocampal volume in older adults. We suggest that the dynamic balance between the hypothalamic-pituitary adrenal axis and inflammation processes may explain hippocampal volume reductions in older adults better than either set of measures do in isolation.
    Frontiers in Aging Neuroscience 07/2014; 6:153. · 2.84 Impact Factor
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    ABSTRACT: Introduction: Multiple studies associate prenatal and perinatal complications with increased risks for autism spectrum disorders (ASDs). The objectives of this study were to utilize a twin study design to 1) Investigate whether shared gestational and perinatal factors increase concordance for ASDs in twins, 2) Determine whether individual neonatal factors are associated with the presence of ASDs in twins, and 3) Explore whether associated factors may influence males and females differently. Methods: Data from medical records and parent response questionnaires from 194 twin pairs, in which at least one twin had an ASD, were analyzed. Results: Shared factors including parental age, prenatal use of medications, uterine bleeding, and prematurity did not increase concordance risks for ASDs in twins. Among the individual factors, respiratory distress demonstrated the strongest association with increased risk for ASDs in the group as a whole (OR 2.11, 95% CI 1.27-3.51). Furthermore, respiratory distress (OR 2.29, 95% CI 1.12-4.67) and other markers of hypoxia (OR 1.99, 95% CI 1.04-3.80) were associated with increased risks for ASDs in males, while jaundice was associated with an increased risk for ASDs in females (OR 2.94, 95% CI 1.28-6.74). Conclusions: Perinatal factors associated with respiratory distress and other markers of hypoxia appear to increase risk for autism in a subgroup of twins. Future studies examining potential gender differences and additional prenatal, perinatal and postnatal environmental factors are required for elucidating the etiology of ASDs and suggesting new methods for treatment and prevention.
    Journal of Psychiatric Research 07/2014; · 4.09 Impact Factor
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    ABSTRACT: Background: Phelan-McDermid Syndrome (PMDS) is a complex neurodevelopmental disorder characterized by global developmental delay, severely impaired speech, intellectual disability, and an increased risk of Autism Spectrum Disorders (ASDs). PMDS is caused by heterozygous deletions of chromosome 22q13.3. Among the genes in the deleted region is SHANK3, which encodes a protein in the postsynaptic density (PSD). Rare mutations in SHANK3 have been associated with idiopathic ASDs, non-syndromic intellectual disability, and schizophrenia. Although SHANK3 is considered to be the most likely candidate gene for the neurological abnormalities in PMDS patients, the cellular and molecular phenotypes associated with this syndrome in human neurons are unknown. Objectives: To investigate cellular and molecular phenotypes associated with PMDS in human neurons. Methods: We generated induced pluripotent stem cells (iPSCs) from individuals with PMDS and autism and used them to produce functional neurons. We then use elctrophysiology, biochemistry, and molecular biology to characterize the properties of iPSC-derived neurons. Results: We show that PMDS neurons have reduced Shank3 expression and major defects in excitatory but not inhibitory synaptic transmission. Excitatory synaptic transmission in PMDS neurons can be corrected by restoring Shank3 expression or by treating neurons with insulin-like growth factor 1 (IGF1). IGF1 treatment promotes formation of excitatory synapses that lack Shank3 but contain PSD95 and NMDA receptors with fast deactivation kinetics. Conclusions: Our findings provide direct evidence for a disruption in the ratio of cellular excitation and inhibition in PMDS neurons, and point to a molecular pathway that can be recruited to restore it.
    2014 International Meeting for Autism Research; 05/2014
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    ABSTRACT: Background: Autism is a highly heritable neurodevelopmental disorder. Previous studies have found sub-threshold social impairments in siblings of children with ASD, as well as in unaffected twins. Objectives: The primary aim of this investigation was to examine the intellectual and social cognitive functioning of monozygotic and dizygotic twins with ASD, with at least one affected twin. This was part of a larger study examining the behavioral and neural correlates of twins with ASD, their siblings, and neurotypical twin pairs. Methods: Monozygotic and dizygotic same-sex twins with ASD, and age-, gender- matched neurotypical twins between the ages of 6 and 14 years were included. Intellectual functioning was assessed using the Stanford-Binet Intelligence Scales (SB5). Social abilities were assessed using the Social Responsiveness Scale (SRS), the Theory of Mind (ToM) and Affect Recognition (AR) Social Perception subtests of the NEPSY-II, as well as a reading the mind in the eyes (Eyes) task, and a Theory of Mind (Smarties) task. Results: A total of 92 participants were included in this investigation: 24 monozygotic with ASD, 40 dizygotic, and 28 neurotypical twins (12 MZ, and 16 DZ). There was no significant difference in age or gender between groups. Difference scores (Δ= Most severe – least affected) on intellectual and social cognitive measures were compared between MZ and DZ neurotypical pairs. As expected, a significant difference was found on the Δ score between monozygotic and dizygotic ASD twin pairs on the SRS total T-score with a trend toward significance on FSIQ score. When comparing the most severe proband between monozygotic and dizygotic twins, there were no significant differences on intellectual abilities or social cognitive functioning measures. The least severely affected MZ probands performed significantly better than the most severely affected DZ probands on both affect recognition tasks (AR and Eyes). Conclusions: Findings from this study suggest that the most severe probands of MZ and DZ twin pairs do not differ significantly from one another on several clinical measures. Interestingly, the least severely affected MZ probands perform better on measures of affect recognition than the most severely affected DZ probands, raising the question of whether aspects of affect recognition are less heritable. This observation is intriguing, but final conclusions cannot be made in light of the small sample size. These preliminary findings warrant additional investigation to comprehensively examine all aspects of intellectual and social cognition in monozygotic and dizygotic twins with autism of all ages.
    2014 International Meeting for Autism Research; 05/2014
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    ABSTRACT: Background: Using proton magnetic resonance spectroscopy (1H MRS) to examine a variety of brain metabolites in twins provides an opportunity to assess the contributions of genetic inheritance, disease state, as well as confounding factors while controlling for metabolite variability in the population. The present ongoing study looks to elucidate relationships between 1H MRS metabolite levels and clinical features across a cohort of same-sex twin pairs with autism and high variability in disease severity. Objectives: 1) To explore differences and similarities among different brain metabolites in MZ and DZ twins, where at least one sibling serves as a proband with autism, and 2) To evaluate the relationship between clinical features and reliably calculated metabolite levels. Methods: The study aims to recruit 120 same-sex twin pairs, 80 with at least one pair with autism, 40 monozygotic (MZ) and 40 dizygotic (DZ), and 40 typically developing twin pair controls, 20 MZ and 20 DZ. High- resolution MRI and 1H MRS imaging scans are being obtained from all participants. Behavior and cognition are also being assessed to provide specific covariates for neuroimaging variables. Results: In this preliminary examination, data from 45 twin pairs were analyzed (age range: 6-15 yrs; Mean 11.04 years ± SD 3.23). Correlations between clinical measures of social abilities and repetitive/restricted behaviors and differences in N Acetyl Aspartate/Creatine levels between twin pairs were examined and several associations were observed including relationships in caudate and putamen with measures of rigidity/restricted behaviors and social cognition, respectively. Among the present findings, our investigation has found lower levels of NAA correlated with symptoms such as repetitive behaviors (Left Putamen NAA/Cre vs total RBS-R score, 95% CI -0.001 : -0.03), sensory abnormalities (Left Caudate NAA/Cre vs SPQ total, 95% CI -0.001 : -0.03), affect recognition (Right Putamen NAA/Cre vs NEPSY AR raw score, 95% CI 0.02 : 0.41), and social responsiveness (Right Thalamus GCP+PCh/Cre vs SRS raw score, 95% CI 0.01 : 0.98). Conclusions: Findings from this preliminary analysis indicate a relationship in autism between brain metabolites and behavior. These observations appear to be consistent with previous reports. Further analyses including more twin pairs will help further current knowledge metabolite abnormalities and neuroanatomic pathways implicated in autism.
    2014 International Meeting for Autism Research; 05/2014
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    ABSTRACT: Rare copy-number variation (CNV) is an important source of risk for autism spectrum disorders (ASDs). We analyzed 2,446 ASD-affected families and confirmed an excess of genic deletions and duplications in affected versus control groups (1.41-fold, p = 1.0 × 10(-5)) and an increase in affected subjects carrying exonic pathogenic CNVs overlapping known loci associated with dominant or X-linked ASD and intellectual disability (odds ratio = 12.62, p = 2.7 × 10(-15), ∼3% of ASD subjects). Pathogenic CNVs, often showing variable expressivity, included rare de novo and inherited events at 36 loci, implicating ASD-associated genes (CHD2, HDAC4, and GDI1) previously linked to other neurodevelopmental disorders, as well as other genes such as SETD5, MIR137, and HDAC9. Consistent with hypothesized gender-specific modulators, females with ASD were more likely to have highly penetrant CNVs (p = 0.017) and were also overrepresented among subjects with fragile X syndrome protein targets (p = 0.02). Genes affected by de novo CNVs and/or loss-of-function single-nucleotide variants converged on networks related to neuronal signaling and development, synapse function, and chromatin regulation.
    The American Journal of Human Genetics 04/2014; · 11.20 Impact Factor
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    ABSTRACT: There is an urgent need for expanding and enhancing autism spectrum disorder (ASD) samples, in order to better understand causes of ASD.
    Molecular Autism 01/2014; 5:34. · 5.49 Impact Factor
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    ABSTRACT: Brain-derived neurotrophic factor (BDNF) protein has been implicated in the pathophysiology of mood disorders, with early data suggesting that blood levels may vary by severity of mood symptoms. BDNF polymorphism, val66met, has also been implicated in mood disorders. Euthymic women with bipolar disorder (BD) (n=47) and healthy control women (n=26), ages 18-45, were clinically rated using the Montgomery-Asberg Depression Rating Scale (MADRS) and sampled for plasma BDNF concentration, with a subset undergoing genetic analysis for the val66met. BD and control groups did not differ on any demographic variables, nor in plasma BDNF levels or val66met polymorphism. Plasma BDNF concentration did not differ by val66met or BD subtype, nor was it correlated with age or illness duration. Within women with BD, lower plasma BDNF concentrations were significantly associated with higher MADRS scores, even after controlling for psychotropic medication use and illness duration. The sample was relatively small and exclusive to women, with further research needed to investigate the links between BDNF markers and mood symptom severity in both men and women. The study provides a gender-specific investigation of plasma BDNF levels and mood, and the results add further evidence of a significant interplay between BDNF markers and psychiatric symptomatology. Further, this association did not appear to be confounded by use of psychotropic medication. Studies with larger samples of both genders are needed to further delineate this relationship.
    Journal of Affective Disorders 12/2013; · 3.76 Impact Factor
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    ABSTRACT: Phelan-McDermid syndrome (PMDS) is a complex neurodevelopmental disorder characterized by global developmental delay, severely impaired speech, intellectual disability, and an increased risk of autism spectrum disorders (ASDs). PMDS is caused by heterozygous deletions of chromosome 22q13.3. Among the genes in the deleted region is SHANK3, which encodes a protein in the postsynaptic density (PSD). Rare mutations in SHANK3 have been associated with idiopathic ASDs, non-syndromic intellectual disability, and schizophrenia. Although SHANK3 is considered to be the most likely candidate gene for the neurological abnormalities in PMDS patients, the cellular and molecular phenotypes associated with this syndrome in human neurons are unknown. We generated induced pluripotent stem (iPS) cells from individuals with PMDS and autism and used them to produce functional neurons. We show that PMDS neurons have reduced SHANK3 expression and major defects in excitatory, but not inhibitory, synaptic transmission. Excitatory synaptic transmission in PMDS neurons can be corrected by restoring SHANK3 expression or by treating neurons with insulin-like growth factor 1 (IGF1). IGF1 treatment promotes formation of mature excitatory synapses that lack SHANK3 but contain PSD95 and N-methyl-d-aspartate (NMDA) receptors with fast deactivation kinetics. Our findings provide direct evidence for a disruption in the ratio of cellular excitation and inhibition in PMDS neurons, and point to a molecular pathway that can be recruited to restore it.
    Nature 10/2013; · 42.35 Impact Factor
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    ABSTRACT: Previous studies in narcolepsy, an autoimmune disorder affecting hypocretin (orexin) neurons and recently associated with H1N1 influenza, have demonstrated significant associations with five loci. Using a well-characterized Chinese cohort, we refined known associations in TRA@ and P2RY11-DNMT1 and identified new associations in the TCR beta (TRB@; rs9648789 max P = 3.7×10(-9) OR 0.77), ZNF365 (rs10995245 max P = 1.2×10(-11) OR 1.23), and IL10RB-IFNAR1 loci (rs2252931 max P = 2.2×10(-9) OR 0.75). Variants in the Human Leukocyte Antigen (HLA)- DQ region were associated with age of onset (rs7744020 P = 7.9×10(-9) beta -1.9 years) and varied significantly among cases with onset after the 2009 H1N1 influenza pandemic compared to previous years (rs9271117 P = 7.8×10(-10) OR 0.57). These reflected an association of DQB1*03:01 with earlier onset and decreased DQB1*06:02 homozygosity following 2009. Our results illustrate how genetic association can change in the presence of new environmental challenges and suggest that the monitoring of genetic architecture over time may help reveal the appearance of novel triggers for autoimmune diseases.
    PLoS Genetics 10/2013; 9(10):e1003880. · 8.17 Impact Factor
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    ABSTRACT: Most psychiatric disorders are moderately to highly heritable. The degree to which genetic variation is unique to individual disorders or shared across disorders is unclear. To examine shared genetic etiology, we use genome-wide genotype data from the Psychiatric Genomics Consortium (PGC) for cases and controls in schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD). We apply univariate and bivariate methods for the estimation of genetic variation within and covariation between disorders. SNPs explained 17–29% of the variance in liability. The genetic correlation calculated using common SNPs was high between schizophrenia and bipolar disorder (0.68 ± 0.04 s.e.), moderate between schizophrenia and major depressive disorder (0.43 ± 0.06 s.e.), bipolar disorder and major depressive disorder (0.47 ± 0.06 s.e.), and ADHD and major depressive disorder (0.32 ± 0.07 s.e.), low between schizophrenia and ASD (0.16 ± 0.06 s.e.) and non-significant for other pairs of disorders as well as between psychiatric disorders and the negative control of Crohn’s disease. This empirical evidence of shared genetic etiology for psychiatric disorders can inform nosology and encourages the investigation of common pathophysiologies for related disorders.
    Nature Genetics 08/2013; AOP. · 29.65 Impact Factor
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    ABSTRACT: There is increasing evidence that genomic imprinting, a process by which certain genes are expressed in a parent-of-origin-specific manner, can influence neurogenetic and psychiatric manifestations. While some data suggest possible imprinting effects of the X chromosome on physical and cognitive characteristics in humans, there is no compelling evidence that X-linked imprinting affects brain morphology. To address this issue, we investigated regional cortical volume, thickness, and surface area in 27 healthy controls and 40 prepubescent girls with Turner syndrome (TS), a condition caused by the absence of one X chromosome. Of the young girls with TS, 23 inherited their X chromosome from their mother (X(m)) and 17 from their father (X(p)). Our results confirm the existence of significant differences in brain morphology between girls with TS and controls, and reveal the presence of a putative imprinting effect among the TS groups: girls with X(p) demonstrated thicker cortex than those with X(m) in the temporal regions bilaterally, while X(m) individuals showed bilateral enlargement of gray matter volume in the superior frontal regions compared with X(p). These data suggest the existence of imprinting effects of the X chromosome that influence both cortical thickness and volume during early brain development, and help to explain variability in cognitive and behavioral manifestations of TS with regard to the parental origin of the X chromosome.
    Journal of Neuroscience 05/2013; 33(19):8567-74. · 6.75 Impact Factor
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    ABSTRACT: Recent advances in the identification of susceptibility genes and environmental exposures provide broad support for a post-infectious autoimmune basis for narcolepsy/hypocretin (orexin) deficiency. We genotyped loci associated with other autoimmune and inflammatory diseases in 1,886 individuals with hypocretin-deficient narcolepsy and 10,421 controls, all of European ancestry, using a custom genotyping array (ImmunoChip). Three loci located outside the Human Leukocyte Antigen (HLA) region on chromosome 6 were significantly associated with disease risk. In addition to a strong signal in the T cell receptor alpha (TRA@), variants in two additional narcolepsy loci, Cathepsin H () and Tumor necrosis factor (ligand) superfamily member 4 (, also called ), attained genome-wide significance. These findings underline the importance of antigen presentation by HLA Class II to T cells in the pathophysiology of this autoimmune disease.
    PLoS Genetics 02/2013; 9(2):e1003270. · 8.17 Impact Factor
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    ABSTRACT: To determine the genetic relationship between head circumference (HC) and Autism Spectrum Disorders (ASDs). Twin pairs with at least one twin with an ASD were assessed. HCs in affected and unaffected individuals were compared, as were HC correlations in monozygotic and dizygotic pairs. 404 subjects, ages 4-18, were included. 20 % of males and 27 % of females with an ASD had macrocephaly. Unaffected co-twins showed similar rates (16 % of males and 22 % of females). Statistical analysis revealed no significant difference in HCs between affected and unaffected twins. Twins with ASDs and unaffected co-twins have similar HCs and increased rates of macrocephaly. Correlations demonstrated partial inheritance of HCs. Thus, macrocephaly may represent an endophenotype in ASDs.
    Journal of Autism and Developmental Disorders 01/2013; · 3.06 Impact Factor
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    ABSTRACT: BACKGROUND: Gene-environment interactions may contribute to bipolar disorder (BD) clinical course variability. We examined effects of brain-derived neurotrophic factor (BDNF) val66met genotype and early life stress (ELS) upon illness severity and chronicity in adult BD patients. METHODS: 80 patients (43 BD I, 33 BD II, 4 BD not otherwise specified, mean ± SD age 46.4 ± 14.0 years, 63.7% female) receiving open evidence-based and measurement-based care in the Stanford Bipolar Disorders Clinic for at least 12 months underwent BDNF val66met genotyping and completed the Childhood Trauma Questionnaire. BDNF met allele carrier genotype and history of childhood sexual and physical abuse were evaluated in relation to mean prior-year Clinical Global Impressions-Bipolar Version-Overall Severity of Illness (MPY-CGI-BP-OS) score and clinical and demographic characteristics. RESULTS: BDNF met allele carriers (but not non-met allele carriers) with compared to without childhood sexual abuse had 21% higher MPY-CGI-BP-OS scores (3.5 ± 0.7 versus 2.9 ± 0.7, respectively, t = -2.4, df = 28, p = 0.025) and 35% earlier BD onset age (14.6 ± 5.7 versus 22.8 ± 7.9 years, respectively, t = 3.0, df = 27, p = 0.006). Regression analysis, however, was non-significant for a BDNF-childhood sexual abuse interaction. LIMITATIONS: small sample of predominantly female Caucasian insured outpatients taking complex medication regimens; only one gene polymorphism considered. CONCLUSIONS: Between group comparisons suggested BDNF met allele carrier genotype might amplify negative effects of ELS upon BD illness severity/chronicity, although with regression analysis, there was not a significant gene-environment interaction. Further studies with larger samples are warranted to assess whether BDNF met allele carriers with ELS are at risk for more severe/chronic BD illness course.
    Journal of Psychiatric Research 11/2012; · 4.09 Impact Factor
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    ABSTRACT: While it is apparent that rare variation can play an important role in the genetic architecture of autism spectrum disorders (ASDs), the contribution of common variation to the risk of developing ASD is less clear. To produce a more comprehensive picture, we report Stage 2 of the Autism Genome Project genome-wide association study, adding 1301 ASD families and bringing the total to 2705 families analysed (Stages 1 and 2). In addition to evaluating the association of individual single nucleotide polymorphisms (SNPs), we also sought evidence that common variants, en masse, might affect the risk. Despite genotyping over a million SNPs covering the genome, no single SNP shows significant association with ASD or selected phenotypes at a genome-wide level. The SNP that achieves the smallest P-value from secondary analyses is rs1718101. It falls in CNTNAP2, a gene previously implicated in susceptibility for ASD. This SNP also shows modest association with age of word/phrase acquisition in ASD subjects, of interest because features of language development are also associated with other variation in CNTNAP2. In contrast, allele scores derived from the transmission of common alleles to Stage 1 cases significantly predict case status in the independent Stage 2 sample. Despite being significant, the variance explained by these allele scores was small (Vm< 1%). Based on results from individual SNPs and their en masse effect on risk, as inferred from the allele score results, it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest.
    Human Molecular Genetics 07/2012; 21(21):4781-92. · 6.68 Impact Factor

Publication Stats

7k Citations
1,187.66 Total Impact Points

Institutions

  • 1994–2014
    • Stanford University
      • • Department of Psychiatry and Behavioral Sciences
      • • Division of Child and Adolescent Psychiatry
      • • Department of Psychology
      • • Department of Genetics
      Palo Alto, California, United States
    • Children's Hospital Los Angeles
      • Division of Psychiatry
      Los Angeles, California, United States
  • 1992–2014
    • Stanford Medicine
      • • Department of Psychiatry and Behavioral Sciences
      • • Department of Genetics
      Stanford, California, United States
  • 2013
    • Peking University People's Hospital
      Peping, Beijing, China
  • 2012
    • Technische Universität München
      München, Bavaria, Germany
  • 2010
    • Trinity College Dublin
      • Department of Psychiatry
      Dublin, L, Ireland
  • 1998–2008
    • University of Western Australia
      • • School of Psychology
      • • School of Psychiatry and Clinical Neurosciences
      • • School of Surgery
      • • Centre for Clinical Research in Neuropsychiatry
      Perth City, Western Australia, Australia
  • 2004–2007
    • Curtin University Australia
      • School of Psychology and Speech Pathology
      Bentley, Western Australia, Australia
  • 2006
    • Griffith University
      • School of Applied Psychology
      Brisbane, Queensland, Australia
    • Case Western Reserve University
      • Department of Epidemiology and Biostatistics
      Cleveland, OH, United States
  • 2004–2006
    • University of Oxford
      • Department of Experimental Psychology
      Oxford, ENG, United Kingdom
  • 1996–2004
    • University of Bonn
      • Institute of Human Genetics
      Bonn, North Rhine-Westphalia, Germany
  • 2001
    • Massachusetts General Hospital
      • Department of Psychiatry
      Boston, MA, United States
  • 2000
    • Western Australia Health
      Perth City, Western Australia, Australia
  • 1999–2000
    • Hollywood Private Hospital
      Perth City, Western Australia, Australia
    • University of Freiburg
      Freiburg, Baden-Württemberg, Germany
  • 1992–1996
    • Johannes Gutenberg-Universität Mainz
      Mayence, Rheinland-Pfalz, Germany
  • 1995
    • Palo Alto Research Center
      Palo Alto, California, United States