对立违抗障碍生物学研究进展
Oppositional Defiant Disorder to Biological Research
DOI: 10.12677/IJPN.2012.14009, PDF, HTML, XML, 下载: 3,232  浏览: 14,315  科研立项经费支持
作者: 王长虹, 宁秋芬, 刘 蒙, 王东平, 李 晏*:新乡医学院第二附属医院;杨 俊*:新乡医学院药学院
关键词: 对立违抗障碍生物学基因综述Oppositional Defiant Disorder; Biology; Gene; Review
摘要: 本文从流行病学特征、母孕期和围生期的不利因素、遗传学研究三方面概述了对立违抗障碍的生物学因素研究进展,并认为其发生发展与遗传因素密切相关,通过基因研究可以提供其易感基因,从而从生物学角度为疾病的预防和治疗提供帮助。
Abstract: This article provided an overview of Oppositional Defiant Disorder research progress of biological factors, from the epidemiological characteristics, the adverse factors during the pregnancy and prenatal period, and genetic research these three aspects, and believed that its development was closely related to genetic factors. Through genetic research could provide its susceptibility gene, which provided help for the prevention and treatment of diseases from a biological perspective.
文章引用:王长虹, 宁秋芬, 刘蒙, 王东平, 李晏, 杨俊. 对立违抗障碍生物学研究进展[J]. 国际神经精神科学杂志, 2012, 1(4): 37-42. http://dx.doi.org/10.12677/IJPN.2012.14009

参考文献

[1] D. M. Fergusson, L. J. Horwood and M. T. Lynskey. Structure of DSM-Ⅲ-R criteria for disruptive childhood behaviors: Confir- matory factor models. Journal of the American Academy of Child and Adolescent Psychiatry, 1994, 33: 1145.
[2] 孙凌, 苏林雁. 长沙市中小学生对立违抗性障碍的现况及对照研究[J]. 中华精神科杂志, 2001, 34(4): 208-211.
[3] T. Ford, R. Goodman and H. Meltzer. The British child and adolescent mental health survey 1999: The prevalence of DSM-IV disorders. Journal of the American Academy of Child and Adolescent Psychiatry, 2003, 42(10): 1203-1211.
[4] M. Zoccolillo, R. Tremblay and F. Vitaro. DSM-III-R and DSM- III criteria for conduct disorder in preadolescent girls: Specific but insensitive. Journal of the American Academy of Child and Adolescent Psychiatry, 1996, 35(4): 461-470.
[5] G. Canino, P. E. Shrout, M. Rubio-Stipec, et al. The DSM-IV rates of child and adolescent disorders in Puerto Rico: Preva- lence, correlates, service use and the effects of impairment. Ar- chives of General Psychiatry, 2004, 61(1): 85-93.
[6] E. E. Ersan, O. Dogan, S. Dogan, et al. The distribution of symptoms of attention-deficit/hyperactivity disorder and oppose- tional defiant disorder in school age children in Turkey. Euro- pean Child & Adolescent Psychiatry, 2004, 13(6): 354-361.
[7] P. S. Jensen, D. Martin and D. P. Cantwell. Comorbidity in ADHD implication for research. Practice and DSM-IV. Journal of the American Academy of Child and Adolescent Psychiatry, 1997, 36: 1065-1079.
[8] 孙凌, 苏林雁, 刘永忠. 长沙市中小学生对立违抗障碍的现况及对照研究[J]. 中华精神科杂志, 2001, 34(4): 208-211.
[9] R. S. Kahn, J. Khoury, W. C. Nichols, et al. Role of dopamine transporter genotype and maternal prenatal smoking in child- hood hyperactive-impulsive, inattentive, and oppositional beha- viors. Journal of Pediatrics, 2003, 143(1): 104-110.
[10] L. Paqani, B. Boulerice, R. E. Tremblay, et al. Behavioural deve- lopment in children of divorce and remarriage. Journal of Child Psychology and Psychiatry, 1997, 38((7): 769-781.
[11] M. C. McCormick, K. Workman-Daniels and J. Brooks-Gunn. The behavioral and emotional wellbeing of school-age children with different birth weights. Pediatrics, 1996, 97(1): 18-25.
[12] M. Wasserman, L. David, B. Wachbroit, et al. Genetics and cri- minal behavior. Cambridge: Cambridge University Press, 2001: 335.
[13] S. R. Jaffee, T. E. Moffitt, A. Caspi, et al. Influence of adult domestic violence on children’s internalizing and externalizing problems: An environmentally informative twin study. Journal of the American Academy of Child and Adolescent Psychiatry, 2002, 41(9): 1095-1103.
[14] R. J. Nelson, S. Chiavegatto. Molecular basis of aggression. Trends in Neurosciences, 2001, 24(12): 713-719.
[15] S. B. Manuck, J. D. Flory, R. E. Ferrell, et al. A regulatory poly- morphism of the monoamine oxidase-A gene may be associated with variability in aggression impulsivity and central nervous system serotonergic responsivity. Psychiatry Research, 2000, 24(1): 9-23.
[16] A. Holmes, D. L. Murphy and J. N. Crawley. Reduced aggres- sion in mice lacking the serotonin transporter. Psychopharma- cology, 2002, 161(2): 160-167.
[17] U. W. Preuss, M. Soyka, M. Bahlmann, et al. Serotonin trans- porter gene regulatory region polymorphism (5-HTTLPR), [3H] paroxetine binding in healthy control subjects and alcohol-de- pendent patients and their relationships to impulsivity. Psychia- try Research, 2000, 96(1): 51-61.
[18] D. E. Comings, R. Gade-Andavolu, N. Gonzalez, et al. Multi- variate analysis of associations of 42 genes in ADHD, ODD and conduct disorder. Clinical Genetics, 2000, 58(1): 31-40.
[19] D. E. Comings, R. Gade-Andavolu, N. Gonzalez, et al. Compar- ison of the role of dopamine, serotonin, and noradrenaline genes in ADHD, ODD and conduct disorder: Multivariate regression analysis of 20 genes. Clinical Genetics, 2000, 57(3): 178-196.
[20] F. L. Coolidge, L. L. Thede and S. E. Young. Heritability and the comorbidity of attention deficit hyperactivity disorder with be- havioral disorders and executive function deficits: A preliminary investigation. Developmental Neuropsychology, 2000, 17(3): 273-287.
[21] L. Eaves, M. Rutter, J. L. Silberg, et al. Genetic and environ- mental causes of covariation in interview assessments of disrupt- tive behavior in child and adolescent twins. Behavior Genetics, 2000, 30(4): 321-334.
[22] 苏林雁, 谢光荣, 高雪屏等. 注意缺陷多动障碍合并对立违抗性障碍患儿血清5羟色胺的对照研究[J]. 中华精神科杂志, 2001, 34(4): 230.
[23] A. Kirley, N. Lowe, C. Mullins, et al. Phenotype studies of the DRD4 gene polymorphisms in ADHD: Association with oppose- tionaldefiant disorder and positive family history. American Journal of Medical Genetics Part B: Neuropsychiatric, 2004, 131B(1): 38-42.
[24] R. K. McHugh, S. G. Hofmann, A. Asnaani, et al. The serotonin transporter gene and risk for alcohol dependence: A meta-ana- lytic review. Drug and Alcohol Dependence, 2010, 108(1-2): 1-6.
[25] J. E. Pirkis, P. M. Burgess, A. K. Johnston, et al. Use of selective serotonin reuptake inhibitors and suicidal ideation: findings from the 2007 National Survey of Mental Health and Wellbeing. Medicine, 2010. 192(1): 53.
[26] N. Nordquist, L. Oreland. Serotonin, genetic variability, behave- iour, and psychiatric disorders: A review. Medical Science, 2010, 115(1): 2-10.
[27] E. H. Kang, H. B. Shim, K. J. Kim, et al. Platelet serotonin transporter function after short-term paroxetine treatment in pa- tients with panic disorder. Psychiatry Research, 2010, 176(2-3): 250-253.
[28] F. F. Rocha, L. A. Marco, M. A. Romano-Silva, et al. Obsessive- compulsive disorder and 5-HTTLPR. Revista Brasileira de Psiquiatria, 2009, 31(3): 287-288.
[29] D. I. Zafeiriou, A. Ververi and E. Vargiami. The serotonergic system: Its role in pathogenesis and early developmental treat- ment of autism. Current Neuropharmacology, 2009, 7(2): 150-157.
[30] D. Marazziti, S. Baroni, I. Masala, et al. Impulsivity, gender, and the platelet serotonin transporter in healthy subjects. Journal of Neuropsychiatric Disease and Treatment, 2010, 6: 9-15.
[31] J. A. Brewer, M. N. Potenza, et al. The neurobiology and genet- ics of impulse control disorders: Relationships to drug addic- tions. Biochemical Pharmacology, 2008, 75(1): 63-65.
[32] E. F. Coccaro, R. Lee. Cerebrospinal fluid 5-hydroxyindolacetic acid and homovanillic acid: Reciprocal relationships with im- pulsive aggression in human subjects. Neural Transmission, 2010, 117(2): 241-248.
[33] H. K. Yoon, Y. K. Kim. Association between serotonin-related gene polymorphisms and suicidal behavior in depressive patients. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 2008, 32(5): 1293-1297.
[34] D. J. Walther, J. U. Peter, S. Bashammakh, et al. Synthesis of serotonin by a second tryptophan hydroxylase isoform. Science, 2003, 299(5603): 76.
[35] D. J. Walther, M. Bader. A unique central tryptophan hydroxyl- lase isoform. Biochemical Pharmacology, 2003, 66(9): 1673- 1680.
[36] X. Zhang, J. M. Beaulieu, T. D. Sotnikova, et al. Tryptophan hydroxylase-2 controls brain serotonin synthesis. Science, 2004, 305(5681): 217.
[37] P. Zill, U. W. Preuss, G. Koller, et al. SNP and haplotype analy- sis of the tryptophan hydroxylase 2 gene in alcohol-dependent patients and alcohol-related suicide. Neuropsychopharmacology, 2007, 32: 1687-1694.
[38] C. L. de Lara, J. Brezo, G. Rouleau, et al. Effect of tryptophan hydroxylase-2 gene variants on suicide risk in major depression. Biological Psychiatry, 2007, 62: 72-80.
[39] H. K. Yoon, Y. K. Kim. TPH2-703G/T SNP may have important effect on susceptibility to suicidal behavior in major depression. Prog Neuropsychopharmacol Biological Psychiatry, 2009, 33(3): 403-409.
[40] T, Banaschewski, K, Becker, S, Scherag, et al. Molecular genet- ics of attention deficit/hyperactivity disorder: An overview. Eur- opean Child & Adolescent Psychiatry, 2010, 19(3): 237-257.
[41] R. D. Oades, S. J. Lasky, H. Christiansen, et al. The influence of serotonin- and other genes on impulsive behavioral aggression and cognitive impulsivity in children with attention-deficit/hy- peractivity disorder (ADHD): Findings from a family-based as- sociation test (FBAT) analysis. Behavioral and Brain Functions, 2008, 4: 48.
[42] R. Sacco, V. Papaleo, J. Hager, et al. Case-control and family- based association studies of candidate genes in autistic disorder and its endophenotypes: TPH2 and GLO1. BMC Medical Ge- netics, 2007, 8: 11.
[43] S. B. Campos, D. M. Miranda, B. R. Souza, et al. Association of polymorphisms of the tryptophan hydroxylase 2 gene with risk for bipolar disorder or suicidal behavior. Journal of Psychiatric Research, 2010, 44(5): 271-274.
[44] R. Y. Ha, K. Namkoong, J. I. Kang, et al. Interaction between serotonin transporter promoter and dopamine receptor D4 poly- morphisms on decision making. Progress in Neuro-Psychophar- macology & Biological Psychiatry, 2009, 33(7): 1217-1222.
[45] T. Fowlera, K. Langleya, et al. Psychopathy trait scores in ado- lescents with childhood ADHD: The contribution of genotypes affecting MAOA, 5HTT and COMT activity. Psychiatric Genet- ics, 2009, 19(6): 312-319.
[46] A. Friseh, B. Finkel and E. Michaelovsky. A rare short allele of the Serotonin transporter Promoter region (5-HTTLPR) found in an aggressive schiz-ophrenic patient of Jewish Libyan origin. Psychiatric Genetics, 2000, 10(4): 179-183.
[47] L. S. Danielle, B. G. Pollock, A. S. Robert, et al. The 5- HTTPR*S/*L polymorphism and aggressive behavior in Alz- heimer disease. Archives of Neurology, 2001, 58(9): 1425-1428.
[48] D. Li, L. He. Meta-analysis supports association between sero- tonin transporter (5-HTT) and suicidal behavior. Molecular Psy- chiatry, 2007, 12(1): 47-54.
[49] G. Pungercica, A. Videtica, et al. Serotonin transporter gene pro- moter (5-HTTLPR) and intron 2(VNTR) polymorphisms: A study on Slovenian population of suicide victims. Psychiatric Genetics, 2006, 16: 187-191.
[50] H. Snoek, S. H. van Goozen, W. Matthys, et al. Serotonergic functioning in children with oppositional defiant disorder: A sumatriptan challenge study. Biological Psychiatry, 2002, 51(4): 319-325.
[51] E. H. Grevet, F. Z. Marques, C. A. Salgado, et al. Serotonin transporter gene polymorphism and the phenotypic heterogene- ity of adult ADHD. Neural Transmission, 2007, 114(12): 1631- 1636.
[52] O. Cases, I. Seif, P. Gaspar, et al. Aggressive behavior and alter- ed amounts of brain serotonin and norepinephrine in mice lack- ing MAOA. Science, 1995, 268: 1763-1766.
[53] M. K. Lai, S. W. Tsang, P. T. Francis, et al. Reduced serotonin 5-HT2A receptor binding in the temporal cortex correlates with aggressive behavior in Alzheimer disease. Brain Research, 2003, 974: 82-87.
[54] J. Biederman, J. W. Kim, A. E. Doyle, et al. Sexually dimorphic effects of four genes (COMT, SLC6A2, MAOA, SLC6A4) in genetic associations of ADHD: A preliminary study. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 2008, 147B(8): 1511-1518.
[55] I. Manor, S. Tyano, E. Mel, J. Eisenberg, et al. Family-based and association studies of monoamine oxidase A and attention deficit hyperactivity disorder(ADHD): Preferential transmission of the long promoter-region repeat and its association with impaired performance on a continuous performance test (TOVA). Molecular Psychiatry, 2002, 7(6): 626-632.
[56] D. Katharine, S. Karen, L. Naomi, et al. Association analysis of the monoamine oxidase A and B genes with attention deficit hyperactivity disorder (ADHD) is an Irish sample; preferential transmission of the MAO-A941G allele to affected children. Journal of Medical Genetics, 2005, 134B(1): 110-114.
[57] I. W. Craiq. The importance of stress and genetic variation in human aggression. Bioessays, 2007, 29(3): 227-236.
[58] K. Malmberg, H. L. Wargelius, P. Lichtenstein, et al. ADHD and disruptive behavior scores—associations with MAO-A and 5-HTT genes and with platelet MAO-B activity in adolescents. Psychiatry, 2008, 23: 8-28.
[59] J. Li, C. Kanq, H. Zhang, et al. Monoamine oxidase A gene polymorphism predicts adolescent outcome of attention-deficit/ hyperactivity disorder. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 2007, 144B(4): 430-433
[60] L. Guan, B. Wanq, et al. A high-density single-nucleotide polymorphism screen of 23 candidate genes in attention deficit hyperactivity disorder: Suggesting multiple susceptibility genes among Chinese Han population. Molecular Psychiatry, 2009, 14(5): 546-554.
[61] I. M. Reti, J. Yanofski, et al. Monoamine oxidase A regulates antisocial personality in whites with no history of physical abuse. Comprehensive Psychiatry, 2011, 52(2): 188-194.
[62] J. M. Esther, B. A. vander Vegta, et al. High activity of monoamine oxidase A is associated with externalizing behaviour in maltreated and nonmaltreated adoptees. Psychiatric Genetics, 2009, 19(4): 209-211.
[63] E. C. Prom-Wormley, L. J. Eaves, et al. Monoamine oxidase A and childhood adversity as risk factors for conduct disorder in females. Psychological Medicine, 2009, 39(4): 579-590.