Skip to main content
Top
Published in: Behavioral and Brain Functions 1/2015

Open Access 01-12-2015 | Review

Expanding the toolbox of ADHD genetics. How can we make sense of parent of origin effects in ADHD and related behavioral phenotypes?

Authors: Tetyana Zayats, Stefan Johansson, Jan Haavik

Published in: Behavioral and Brain Functions | Issue 1/2015

Login to get access

Abstract

Genome-wide association (GWA) studies have shown that many different genetic variants cumulatively contribute to the risk of psychiatric disorders. It has also been demonstrated that various parent-of-origin effects (POE) may differentially influence the risk of these disorders. Together, these observations have provided important new possibilities to uncover the genetic underpinnings of such complex phenotypes. As POE so far have received little attention in neuropsychiatric disorders, there is still much progress to be made. Here, we mainly focus on the new and emerging role of POE in attention-deficit hyperactivity disorder (ADHD). We review the current evidence that POE play an imperative role in vulnerability to ADHD and related disorders. We also discuss how POE can be assessed using statistical genetics tools, expanding the resources of modern psychiatric genetics. We propose that better comprehension and inspection of POE may offer new insight into the molecular basis of ADHD and related phenotypes, as well as the potential for preventive and therapeutic interventions.
Literature
1.
go back to reference Schizophrenia Working Group of the Psychiatric Genomics C. Biological insights from 108 schizophrenia-associated genetic loci. Nature. 2014;511(7510):421–7.CrossRef Schizophrenia Working Group of the Psychiatric Genomics C. Biological insights from 108 schizophrenia-associated genetic loci. Nature. 2014;511(7510):421–7.CrossRef
2.
go back to reference Faraone SV, et al. Molecular genetics of attention-deficit/hyperactivity disorder. Biol Psych. 2005;57(11):1313–23.CrossRef Faraone SV, et al. Molecular genetics of attention-deficit/hyperactivity disorder. Biol Psych. 2005;57(11):1313–23.CrossRef
3.
go back to reference Polanczyk G, et al. The worldwide prevalence of ADHD: a systematic review and metaregression analysis. Am J Psych. 2007;164(6):942–8.CrossRef Polanczyk G, et al. The worldwide prevalence of ADHD: a systematic review and metaregression analysis. Am J Psych. 2007;164(6):942–8.CrossRef
4.
go back to reference Kebir O, et al. Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies. J Psych Neurosci. 2009;34(2):88–101. Kebir O, et al. Candidate genes and neuropsychological phenotypes in children with ADHD: review of association studies. J Psych Neurosci. 2009;34(2):88–101.
5.
go back to reference Ainsworth HF, et al. Investigatio of maternal effects, maternal-fetal interactions and parent-of-origin effects (imprinting), using mothers and their offspring. Genet Epidemiol. 2011;35:19–45.PubMedCentralCrossRefPubMed Ainsworth HF, et al. Investigatio of maternal effects, maternal-fetal interactions and parent-of-origin effects (imprinting), using mothers and their offspring. Genet Epidemiol. 2011;35:19–45.PubMedCentralCrossRefPubMed
6.
go back to reference Buyske S. Maternal genotype effects can alias case genotype effects in case–controls studies. Eur J Hum Genet. 2008;16:784–5.CrossRef Buyske S. Maternal genotype effects can alias case genotype effects in case–controls studies. Eur J Hum Genet. 2008;16:784–5.CrossRef
7.
go back to reference Curley JP, Mashoodh R. Parent-of-origin and trans-generational germline influences on behavioral development: the interacting roles of mothers, fathers, and grandparents. Dev Psychobiol. 2010;52(4):312–30.CrossRefPubMed Curley JP, Mashoodh R. Parent-of-origin and trans-generational germline influences on behavioral development: the interacting roles of mothers, fathers, and grandparents. Dev Psychobiol. 2010;52(4):312–30.CrossRefPubMed
9.
go back to reference Reik W, Walter J. Genomic imprinting: parental influence on the genome. Nat Rev Genet. 2001;2(1):21–32.CrossRefPubMed Reik W, Walter J. Genomic imprinting: parental influence on the genome. Nat Rev Genet. 2001;2(1):21–32.CrossRefPubMed
10.
go back to reference de la Casa-Esperon E, Sapienza C. Natural selection and the evolution of genome imprinting. Annu Rev Genet. 2003;37:349–70.CrossRefPubMed de la Casa-Esperon E, Sapienza C. Natural selection and the evolution of genome imprinting. Annu Rev Genet. 2003;37:349–70.CrossRefPubMed
11.
go back to reference Egger G, et al. Epigenetics in human disease and prospects for epigenetic therapy. Nature. 2004;429(6990):457–63.CrossRefPubMed Egger G, et al. Epigenetics in human disease and prospects for epigenetic therapy. Nature. 2004;429(6990):457–63.CrossRefPubMed
12.
go back to reference Jaenisch R, Bird A. Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals. Nat Genet. 2003;33(Suppl):245–54.CrossRefPubMed Jaenisch R, Bird A. Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals. Nat Genet. 2003;33(Suppl):245–54.CrossRefPubMed
13.
14.
go back to reference Isles AR, Wilkinson LS. Imprinted genes, cognition and behaviour. Trend Cogn Sci. 2000;4(8):309–18.CrossRef Isles AR, Wilkinson LS. Imprinted genes, cognition and behaviour. Trend Cogn Sci. 2000;4(8):309–18.CrossRef
15.
go back to reference Pun FW, et al. Imprinting in the schizophrenia candidate gene GABRB2 encoding GABA(A) receptor beta(2) subunit. Mol Psych. 2011;16(5):557–68.CrossRef Pun FW, et al. Imprinting in the schizophrenia candidate gene GABRB2 encoding GABA(A) receptor beta(2) subunit. Mol Psych. 2011;16(5):557–68.CrossRef
16.
go back to reference Ludwig KU, et al. Supporting evidence for LRRTM1 imprinting effects in schizophrenia. Mol Psych. 2009;14(8):743–5.CrossRef Ludwig KU, et al. Supporting evidence for LRRTM1 imprinting effects in schizophrenia. Mol Psych. 2009;14(8):743–5.CrossRef
17.
go back to reference Skuse DH. Imprinting, the X-chromosome, and the male brain: explaining sex differences in the liability to autism. Pediatr Res. 2000;47(1):9–16.CrossRefPubMed Skuse DH. Imprinting, the X-chromosome, and the male brain: explaining sex differences in the liability to autism. Pediatr Res. 2000;47(1):9–16.CrossRefPubMed
18.
go back to reference Badcock C, Crespi B. Imbalanced genomic imprinting in brain development: an evolutionary basis for the aetiology of autism. J Evol Biol. 2006;19(4):1007–32.CrossRefPubMed Badcock C, Crespi B. Imbalanced genomic imprinting in brain development: an evolutionary basis for the aetiology of autism. J Evol Biol. 2006;19(4):1007–32.CrossRefPubMed
19.
go back to reference McMahon FJ, et al. Patterns of maternal transmission in bipolar affective disorder. Am J Hum Genet. 1995;56(6):1277–86.PubMedCentralPubMed McMahon FJ, et al. Patterns of maternal transmission in bipolar affective disorder. Am J Hum Genet. 1995;56(6):1277–86.PubMedCentralPubMed
20.
go back to reference Borglum AD, et al. Possible parent-of-origin effect of Dopa decarboxylase in susceptibility to bipolar affective disorder. Am J Med Genet B Neuropsychiatr Genet. 2003;117B(1):18–22.CrossRefPubMed Borglum AD, et al. Possible parent-of-origin effect of Dopa decarboxylase in susceptibility to bipolar affective disorder. Am J Med Genet B Neuropsychiatr Genet. 2003;117B(1):18–22.CrossRefPubMed
21.
go back to reference Goos LM, Ezzatian P, Schachar R. Parent-of-origin effects in attention-deficit hyperactivity disorder. Psych Res. 2007;149(1–3):1–9.CrossRef Goos LM, Ezzatian P, Schachar R. Parent-of-origin effects in attention-deficit hyperactivity disorder. Psych Res. 2007;149(1–3):1–9.CrossRef
22.
go back to reference Lichter DG, Jackson LA, Schachter M. Clinical evidence of genomic imprinting in Tourette’s syndrome. Neurology. 1995;45(5):924–8.CrossRefPubMed Lichter DG, Jackson LA, Schachter M. Clinical evidence of genomic imprinting in Tourette’s syndrome. Neurology. 1995;45(5):924–8.CrossRefPubMed
23.
go back to reference Crowley JJ, et al. Analyses of allele-specific gene expression in highly divergent mouse crosses identifies pervasive allelic imbalance. Nat Genet. 2015;47(4):353–60.PubMedCentralCrossRefPubMed Crowley JJ, et al. Analyses of allele-specific gene expression in highly divergent mouse crosses identifies pervasive allelic imbalance. Nat Genet. 2015;47(4):353–60.PubMedCentralCrossRefPubMed
24.
go back to reference Jacobsen KK et al. Epistatic and gene wide effects in YWHA and aromatic amino hydroxylase genes across ADHD and other common neuropsychiatric disorders: association with YWHAE. Am J Med Genet B Neuropsychiatr Genet. 2015. Jacobsen KK et al. Epistatic and gene wide effects in YWHA and aromatic amino hydroxylase genes across ADHD and other common neuropsychiatric disorders: association with YWHAE. Am J Med Genet B Neuropsychiatr Genet. 2015.
25.
go back to reference Brophy K, et al. Synaptosomal-associated protein 25 (SNAP-25) and attention deficit hyperactivity disorder (ADHD): evidence of linkage and association in the Irish population. Mol Psych. 2002;7(8):913–7.CrossRef Brophy K, et al. Synaptosomal-associated protein 25 (SNAP-25) and attention deficit hyperactivity disorder (ADHD): evidence of linkage and association in the Irish population. Mol Psych. 2002;7(8):913–7.CrossRef
26.
go back to reference Kustanovich V, et al. Biased paternal transmission of SNAP-25 risk alleles in attention-deficit hyperactivity disorder. Mol Psych. 2003;8(3):309–15.CrossRef Kustanovich V, et al. Biased paternal transmission of SNAP-25 risk alleles in attention-deficit hyperactivity disorder. Mol Psych. 2003;8(3):309–15.CrossRef
27.
go back to reference Mill J, et al. Haplotype analysis of SNAP-25 suggests a role in the aetiology of ADHD. Mol Psych. 2004;9(8):801–10.CrossRef Mill J, et al. Haplotype analysis of SNAP-25 suggests a role in the aetiology of ADHD. Mol Psych. 2004;9(8):801–10.CrossRef
28.
go back to reference Hawi Z, et al. Serotonergic system and attention deficit hyperactivity disorder (ADHD): a potential susceptibility locus at the 5-HT(1B) receptor gene in 273 nuclear families from a multi-centre sample. Mol Psych. 2002;7(7):718–25.CrossRef Hawi Z, et al. Serotonergic system and attention deficit hyperactivity disorder (ADHD): a potential susceptibility locus at the 5-HT(1B) receptor gene in 273 nuclear families from a multi-centre sample. Mol Psych. 2002;7(7):718–25.CrossRef
29.
go back to reference Quist JF, et al. The serotonin 5-HT1B receptor gene and attention deficit hyperactivity disorder. Mol Psych. 2003;8(1):98–102.CrossRef Quist JF, et al. The serotonin 5-HT1B receptor gene and attention deficit hyperactivity disorder. Mol Psych. 2003;8(1):98–102.CrossRef
30.
go back to reference Smoller JW, et al. Association between the 5HT1B receptor gene (HTR1B) and the inattentive subtype of ADHD. Biol Psych. 2006;59(5):460–7.CrossRef Smoller JW, et al. Association between the 5HT1B receptor gene (HTR1B) and the inattentive subtype of ADHD. Biol Psych. 2006;59(5):460–7.CrossRef
31.
go back to reference Hawi Z, et al. Preferential transmission of paternal alleles at risk genes in attention-deficit/hyperactivity disorder. Am J Hum Genet. 2005;77(6):958–65.PubMedCentralCrossRefPubMed Hawi Z, et al. Preferential transmission of paternal alleles at risk genes in attention-deficit/hyperactivity disorder. Am J Hum Genet. 2005;77(6):958–65.PubMedCentralCrossRefPubMed
32.
go back to reference Banerjee E, et al. A family-based study of Indian subjects from Kolkata reveals allelic association of the serotonin transporter intron-2 (STin2) polymorphism and attention-deficit-hyperactivity disorder (ADHD). Am J Med Genet B Neuropsychiatr Genet. 2006;141B(4):361–6.CrossRefPubMed Banerjee E, et al. A family-based study of Indian subjects from Kolkata reveals allelic association of the serotonin transporter intron-2 (STin2) polymorphism and attention-deficit-hyperactivity disorder (ADHD). Am J Med Genet B Neuropsychiatr Genet. 2006;141B(4):361–6.CrossRefPubMed
33.
go back to reference Kent L, et al. Association of the paternally transmitted copy of common Valine allele of the Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene with susceptibility to ADHD. Mol Psych. 2005;10(10):939–43.CrossRef Kent L, et al. Association of the paternally transmitted copy of common Valine allele of the Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene with susceptibility to ADHD. Mol Psych. 2005;10(10):939–43.CrossRef
34.
go back to reference Hawi Z, et al. Dopa decarboxylase gene polymorphisms and attention deficit hyperactivity disorder (ADHD): no evidence for association in the Irish population. Mol Psych. 2001;6(4):420–4.CrossRef Hawi Z, et al. Dopa decarboxylase gene polymorphisms and attention deficit hyperactivity disorder (ADHD): no evidence for association in the Irish population. Mol Psych. 2001;6(4):420–4.CrossRef
35.
go back to reference Laurin N, et al. Investigation of the G protein subunit Galphaolf gene (GNAL) in attention deficit/hyperactivity disorder. J Psychiatr Res. 2008;42(2):117–24.CrossRefPubMed Laurin N, et al. Investigation of the G protein subunit Galphaolf gene (GNAL) in attention deficit/hyperactivity disorder. J Psychiatr Res. 2008;42(2):117–24.CrossRefPubMed
36.
go back to reference Hawi Z, et al. ADHD and DAT1: further evidence of paternal over-transmission of risk alleles and haplotype. Am J Med Genet B Neuropsychiatr Genet. 2010;153B(1):97–102.PubMed Hawi Z, et al. ADHD and DAT1: further evidence of paternal over-transmission of risk alleles and haplotype. Am J Med Genet B Neuropsychiatr Genet. 2010;153B(1):97–102.PubMed
37.
go back to reference Wang KS, et al. Parent-of-origin effects of FAS and PDLIM1 in attention-deficit/hyperactivity disorder. J Psych Neurosci. 2012;37(1):46–52.CrossRef Wang KS, et al. Parent-of-origin effects of FAS and PDLIM1 in attention-deficit/hyperactivity disorder. J Psych Neurosci. 2012;37(1):46–52.CrossRef
38.
go back to reference Connolly S, Heron E. Review of statistical methodologies for the detection of parent-of-origin effects in family trio genome-wide association data with binary disease traits. Brief Bioinform. 2014;16:429–48.CrossRefPubMed Connolly S, Heron E. Review of statistical methodologies for the detection of parent-of-origin effects in family trio genome-wide association data with binary disease traits. Brief Bioinform. 2014;16:429–48.CrossRefPubMed
39.
go back to reference Shumay E, Fowler JS, Volkow ND. Genomic features of the human dopamine transporter gene and its potential epigenetic states: implications for phenotypic diversity. PLoS One. 2010;5(6):e11067.PubMedCentralCrossRefPubMed Shumay E, Fowler JS, Volkow ND. Genomic features of the human dopamine transporter gene and its potential epigenetic states: implications for phenotypic diversity. PLoS One. 2010;5(6):e11067.PubMedCentralCrossRefPubMed
41.
go back to reference Rampersaud E, et al. Investigating parent of origin effects in studies of type 2 diabetes and obesity. Curr Diabet Rev. 2008;4(4):329–39.CrossRef Rampersaud E, et al. Investigating parent of origin effects in studies of type 2 diabetes and obesity. Curr Diabet Rev. 2008;4(4):329–39.CrossRef
43.
go back to reference Haavik J, et al. Maternal genotypes as predictors of offspring mental health: the next frontier of genomic medicine? Futur Neurol. 2011;6(6):731.CrossRef Haavik J, et al. Maternal genotypes as predictors of offspring mental health: the next frontier of genomic medicine? Futur Neurol. 2011;6(6):731.CrossRef
44.
go back to reference Hager R, Cheverud JM, Wolf JB. Change in maternal environment induced by cross-fostering alters genetic and epigenetic effects on complex traits in mice. Proc Biol Sci. 2009;276(1669):2949–54.PubMedCentralCrossRefPubMed Hager R, Cheverud JM, Wolf JB. Change in maternal environment induced by cross-fostering alters genetic and epigenetic effects on complex traits in mice. Proc Biol Sci. 2009;276(1669):2949–54.PubMedCentralCrossRefPubMed
45.
go back to reference Halmoy A, et al. Attention-deficit/hyperactivity disorder symptoms in offspring of mothers with impaired serotonin production. Arch Gen Psych. 2010;67(10):1033–43.CrossRef Halmoy A, et al. Attention-deficit/hyperactivity disorder symptoms in offspring of mothers with impaired serotonin production. Arch Gen Psych. 2010;67(10):1033–43.CrossRef
46.
go back to reference Moses-Kolko EL, et al. Neonatal signs after late in utero exposure to serotonin reuptake inhibitors: literature review and implications for clinical applications. JAMA. 2005;293(19):2372–83.CrossRefPubMed Moses-Kolko EL, et al. Neonatal signs after late in utero exposure to serotonin reuptake inhibitors: literature review and implications for clinical applications. JAMA. 2005;293(19):2372–83.CrossRefPubMed
47.
go back to reference Gleason G, et al. The serotonin1A receptor gene as a genetic and prenatal maternal environmental factor in anxiety. Proc Natl Acad Sci. 2010;107(16):7592–7.PubMedCentralCrossRefPubMed Gleason G, et al. The serotonin1A receptor gene as a genetic and prenatal maternal environmental factor in anxiety. Proc Natl Acad Sci. 2010;107(16):7592–7.PubMedCentralCrossRefPubMed
48.
go back to reference Martorell L, et al. New variants in the mitochondrial genomes of schizophrenic patients. Eur J Hum Genet. 2006;14(5):520–8.CrossRefPubMed Martorell L, et al. New variants in the mitochondrial genomes of schizophrenic patients. Eur J Hum Genet. 2006;14(5):520–8.CrossRefPubMed
52.
go back to reference Schwartz M, Vissing J. Paternal inheritance of mitochondrial DNA. N Engl J Med. 2002;347(8):576–80.CrossRefPubMed Schwartz M, Vissing J. Paternal inheritance of mitochondrial DNA. N Engl J Med. 2002;347(8):576–80.CrossRefPubMed
53.
go back to reference Billups B, Forsythe ID. Presynaptic mitochondrial calcium sequestration influences transmission at mammalian central synapses. J Neurosci. 2002;22(14):5840–7.PubMed Billups B, Forsythe ID. Presynaptic mitochondrial calcium sequestration influences transmission at mammalian central synapses. J Neurosci. 2002;22(14):5840–7.PubMed
54.
go back to reference Kubota M, et al. Abnormal Ca2+ dynamics in transgenic mice with neuron-specific mitochondrial DNA defects. J Neurosci. 2006;26(47):12314–24.CrossRefPubMed Kubota M, et al. Abnormal Ca2+ dynamics in transgenic mice with neuron-specific mitochondrial DNA defects. J Neurosci. 2006;26(47):12314–24.CrossRefPubMed
55.
go back to reference Kiser DP, Rivero O, Lesch KP. Annual research review: the (epi)genetics of neurodevelopmental disorders in the era of whole-genome sequencing–unveiling the dark matter. J Child Psychol Psych. 2015;56(3):278–95.CrossRef Kiser DP, Rivero O, Lesch KP. Annual research review: the (epi)genetics of neurodevelopmental disorders in the era of whole-genome sequencing–unveiling the dark matter. J Child Psychol Psych. 2015;56(3):278–95.CrossRef
56.
go back to reference Olsson M, et al. Mitochondrial haplogroup is associated with the phenotype of familial amyloidosis with polyneuropathy in Swedish and French patients. Clin Genet. 2009;75(2):163–8.CrossRefPubMed Olsson M, et al. Mitochondrial haplogroup is associated with the phenotype of familial amyloidosis with polyneuropathy in Swedish and French patients. Clin Genet. 2009;75(2):163–8.CrossRefPubMed
57.
go back to reference Bonaiti B, et al. Parent-of-origin effect in transthyretin related amyloid polyneuropathy. Amyloid. 2009;16(3):149–50.CrossRefPubMed Bonaiti B, et al. Parent-of-origin effect in transthyretin related amyloid polyneuropathy. Amyloid. 2009;16(3):149–50.CrossRefPubMed
58.
go back to reference Sluyter F, et al. Aggression in wild house mice: current state of affairs. Behav Genet. 1996;26(5):489–96.CrossRefPubMed Sluyter F, et al. Aggression in wild house mice: current state of affairs. Behav Genet. 1996;26(5):489–96.CrossRefPubMed
59.
go back to reference Guillot PV, et al. Hippocampal morphology in the inbred mouse strains NZB and CBA/H and their reciprocal congenics for the nonpseudoautosomal region of the Y chromosome. Behav Genet. 1996;26(1):1–5.CrossRefPubMed Guillot PV, et al. Hippocampal morphology in the inbred mouse strains NZB and CBA/H and their reciprocal congenics for the nonpseudoautosomal region of the Y chromosome. Behav Genet. 1996;26(1):1–5.CrossRefPubMed
61.
go back to reference Gizer IR, Ficks C, Waldman ID. Candidate gene studies of ADHD: a meta-analytic review. Hum Genet. 2009;126(1):51–90.CrossRefPubMed Gizer IR, Ficks C, Waldman ID. Candidate gene studies of ADHD: a meta-analytic review. Hum Genet. 2009;126(1):51–90.CrossRefPubMed
62.
go back to reference Bruining H, et al. The parent-of-origin of the extra X chromosome may differentially affect psychopathology in Klinefelter syndrome. Biol Psych. 2010;68(12):1156–62.CrossRef Bruining H, et al. The parent-of-origin of the extra X chromosome may differentially affect psychopathology in Klinefelter syndrome. Biol Psych. 2010;68(12):1156–62.CrossRef
63.
go back to reference Skuse DH, et al. Evidence from Turner’s syndrome of an imprinted X-linked locus affecting cognitive function. Nature. 1997;387(6634):705–8.CrossRefPubMed Skuse DH, et al. Evidence from Turner’s syndrome of an imprinted X-linked locus affecting cognitive function. Nature. 1997;387(6634):705–8.CrossRefPubMed
64.
65.
66.
67.
go back to reference Hager R, Cheverud JM, Wolf JB. Maternal effects as the cause of parent-of-origin effects that mimic genomic imprinting. Genetics. 2008;178(3):1755–62.PubMedCentralCrossRefPubMed Hager R, Cheverud JM, Wolf JB. Maternal effects as the cause of parent-of-origin effects that mimic genomic imprinting. Genetics. 2008;178(3):1755–62.PubMedCentralCrossRefPubMed
68.
go back to reference Joober R, Sengupta S. Parent-of-origin effect and risk for attention-deficit/hyperactivity disorder: balancing the evidence against bias and chance findings. Am J Hum Genet. 2006;79(4):765–6 (author reply 766–8).PubMedCentralCrossRefPubMed Joober R, Sengupta S. Parent-of-origin effect and risk for attention-deficit/hyperactivity disorder: balancing the evidence against bias and chance findings. Am J Hum Genet. 2006;79(4):765–6 (author reply 766–8).PubMedCentralCrossRefPubMed
69.
go back to reference Laurin N, et al. No preferential transmission of paternal alleles at risk genes in attention-deficit hyperactivity disorder. Mol Psych. 2007;12(3):226–9.CrossRef Laurin N, et al. No preferential transmission of paternal alleles at risk genes in attention-deficit hyperactivity disorder. Mol Psych. 2007;12(3):226–9.CrossRef
70.
go back to reference Anney RJ, et al. Parent of origin effects in attention/deficit hyperactivity disorder (ADHD): analysis of data from the international multicenter ADHD genetics (IMAGE) program. Am J Med Genet B Neuropsychiatr Genet. 2008;147B(8):1495–500.CrossRefPubMed Anney RJ, et al. Parent of origin effects in attention/deficit hyperactivity disorder (ADHD): analysis of data from the international multicenter ADHD genetics (IMAGE) program. Am J Med Genet B Neuropsychiatr Genet. 2008;147B(8):1495–500.CrossRefPubMed
71.
go back to reference Kim JW, et al. Investigation of parent-of-origin effects in ADHD candidate genes. Am J Med Genet B Neuropsychiatr Genet. 2007;144B(6):776–80.CrossRefPubMed Kim JW, et al. Investigation of parent-of-origin effects in ADHD candidate genes. Am J Med Genet B Neuropsychiatr Genet. 2007;144B(6):776–80.CrossRefPubMed
72.
go back to reference Schimmelmann BG, et al. No evidence for preferential transmission of common valine allele of the Val66Met polymorphism of the brain-derived neurotrophic factor gene (BDNF) in ADHD. J Neural Transm. 2007;114(4):523–6.CrossRefPubMed Schimmelmann BG, et al. No evidence for preferential transmission of common valine allele of the Val66Met polymorphism of the brain-derived neurotrophic factor gene (BDNF) in ADHD. J Neural Transm. 2007;114(4):523–6.CrossRefPubMed
73.
go back to reference Weinberg CR, Wilcox AJ, Lie RT. A log-linear approach to case-parent-triad data: assessing effects of disease genes that act either directly or through maternal effects and that may be subject to parental imprinting. Am J Hum Genet. 1998;62(4):969–78.PubMedCentralCrossRefPubMed Weinberg CR, Wilcox AJ, Lie RT. A log-linear approach to case-parent-triad data: assessing effects of disease genes that act either directly or through maternal effects and that may be subject to parental imprinting. Am J Hum Genet. 1998;62(4):969–78.PubMedCentralCrossRefPubMed
74.
go back to reference Gjessing HK, Lie RT. Case-parent triads: estimating single- and double-dose effects of fetal and maternal disease gene haplotypes. Ann Hum Genet. 2006;70(Pt 3):382–96.PubMed Gjessing HK, Lie RT. Case-parent triads: estimating single- and double-dose effects of fetal and maternal disease gene haplotypes. Ann Hum Genet. 2006;70(Pt 3):382–96.PubMed
75.
go back to reference Howey R, Cordell HJ. PREMIM and EMIM: tools for estimation of maternal, imprinting and interaction effects using multinomial modelling. BMC Bioinform. 2012;13:149.CrossRef Howey R, Cordell HJ. PREMIM and EMIM: tools for estimation of maternal, imprinting and interaction effects using multinomial modelling. BMC Bioinform. 2012;13:149.CrossRef
76.
77.
go back to reference Wilcox AJ, Weinberg CR, Lie RT. Distinguishing the effects of maternal and offspring genes through studies of “case-parent triads”. Am J Epidemiol. 1998;148:893–901.CrossRefPubMed Wilcox AJ, Weinberg CR, Lie RT. Distinguishing the effects of maternal and offspring genes through studies of “case-parent triads”. Am J Epidemiol. 1998;148:893–901.CrossRefPubMed
79.
go back to reference Hoggart CJ, et al. Novel approach identifies SNPs in SLC2A10 and KCNK9 with evidence for parent-of-origin effect on body mass index. PLoS Genet. 2014;10(7):e1004508.PubMedCentralCrossRefPubMed Hoggart CJ, et al. Novel approach identifies SNPs in SLC2A10 and KCNK9 with evidence for parent-of-origin effect on body mass index. PLoS Genet. 2014;10(7):e1004508.PubMedCentralCrossRefPubMed
80.
go back to reference Lawlor DA, et al. Mendelian randomization:using genes as intruments for making causal inferences in epidemiology. Stat Med. 2008;27:1133–63.CrossRefPubMed Lawlor DA, et al. Mendelian randomization:using genes as intruments for making causal inferences in epidemiology. Stat Med. 2008;27:1133–63.CrossRefPubMed
81.
go back to reference Zuccolo L, et al. Prenatal alcohol exposure and offspring cognition and school performance. A “Mendelian randomization” natural experiment. Int J Epidem. 2013;42:1358–70.CrossRef Zuccolo L, et al. Prenatal alcohol exposure and offspring cognition and school performance. A “Mendelian randomization” natural experiment. Int J Epidem. 2013;42:1358–70.CrossRef
82.
go back to reference Cross-Disorder Group of the Psychiatric Genomics, C. Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. Lancet. 2013;381(9875):1371–9.CrossRef Cross-Disorder Group of the Psychiatric Genomics, C. Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis. Lancet. 2013;381(9875):1371–9.CrossRef
83.
go back to reference Lehn H, et al. Attention problems and attention-deficit/hyperactivity disorder in discordant and concordant monozygotic twins: evidence of environmental mediators. J Am Acad Child Adolesc Psych. 2007;46(1):83–91.CrossRef Lehn H, et al. Attention problems and attention-deficit/hyperactivity disorder in discordant and concordant monozygotic twins: evidence of environmental mediators. J Am Acad Child Adolesc Psych. 2007;46(1):83–91.CrossRef
Metadata
Title
Expanding the toolbox of ADHD genetics. How can we make sense of parent of origin effects in ADHD and related behavioral phenotypes?
Authors
Tetyana Zayats
Stefan Johansson
Jan Haavik
Publication date
01-12-2015
Publisher
BioMed Central
Published in
Behavioral and Brain Functions / Issue 1/2015
Electronic ISSN: 1744-9081
DOI
https://doi.org/10.1186/s12993-015-0078-4

Other articles of this Issue 1/2015

Behavioral and Brain Functions 1/2015 Go to the issue