童年期虐待与单胺氧化酶A基因多态性在青少年反社会行为中的交互作用

袁梦园; 苏普玉

doi:10.16835/j.cnki.1000-9817.2021.05.036

童年期虐待与单胺氧化酶A基因多态性在青少年反社会行为中的交互作用

doi: 10.16835/j.cnki.1000-9817.2021.05.036

袁梦园,
苏普玉^,

安徽医科大学公共卫生学院儿少卫生与妇幼保健学系/出生人口健康教育部重点实验室/人口健康与优生安徽省重点实验室，合肥，230032

基金项目:

国家自然科学基金面上项目 81874268

详细信息

作者简介:
袁梦园(1997-)，女，安徽六安人，在读硕士，主要研究方向为儿童青少年发育与行为医学

通讯作者:
苏普玉，E-mail: supuyu@ahmu.edu.cn

中图分类号: R 179 G 444 B 844.2
计量
- 文章访问数: 596
- HTML全文浏览量: 328
- PDF下载量: 58
- 被引次数: 0
出版历程
- 收稿日期: 2020-07-08
- 修回日期: 2020-09-20
- 网络出版日期: 2021-05-20
- 刊出日期: 2021-05-25

Research progress for the interaction of child abuse and monoamine oxidase A gene on antisocial behavior among adolescents

YUAN Mengyuan,
SU Puyu^,

Department of Maternal, Child and Adolescent Health, School of Public Health, Anhui Medical University/Key Laboratory of Population Health Across Life Cycle, Ministry of Education of the People's Republic of China/Anhui Provincial Key Laboratory of Population Health and Aristogenics, Hefei(230032), China

摘要

摘要: 青少年反社会行为给个人健康、家庭和社会都带来沉重的负担，引起了公众的广泛关注。目前，大多数研究已证实童年期虐待、单胺氧化酶A基因与反社会行为之间存在关联。然而，关于童年期虐待与单胺氧化酶A基因交互作用与反社会行为之间的关联性尚存在争议。本文旨在对童年期虐待与单胺氧化酶A基因交互作用与青少年反社会行为的最新研究成果及其可能的作用机制进行综述，发现童年期虐待与单胺氧化酶A基因可能通过影响大脑中特定的神经环路、改变情绪调节功能等交互作用于反社会行为。此外，本综述剖析了当前研究结果不一致的可能原因，为今后研究指明方向，也为青少年反社会行为的预防控制提供科学依据。
- 虐待儿童 /
- 基因 /
- 社会行为 /
- 青少年 /
- 精神卫生
Abstract: Antisocial behavior among adolescents caused a severe burden on individuals, families and society, which has aroused a global concern. At present, the association of child abuse and monoamine oxidase A gene with antisocial behavior has been confirmed in most studies. However, there was a controversy about the interaction of child abuse and monoamine oxidase A gene on antisocial behavior. This study aimed to review latest findings and mechanisms of the interaction of child abuse and monoamine oxidase A gene on antisocial behavior among adolescents. The result showed that the child abuse interacted with monoamine oxidase A gene in antisocial behavior by influencing the specific neural circuits in the brain and changing the function of mood regulation, etc. Additionally, this study analyzed potential reasons for the inconsistency of current study findings, and identified the directions for future research. Moreover, this review was to provide a scientific basis for the prevention and control of adolescent antisocial behavior.
- Child abuse /
- Genes /
- Social behavior /
- Adolescent /
- Mental health

HTML全文

参考文献(52)

[1]	吕鹏. 基于预测视角的反社会行为谱系类型与研究述评[J]. 晋阳学刊, 2020, 41(2): 104-114. https://www.cnki.com.cn/Article/CJFDTOTAL-JYXK202002015.htm LYU P. The genealogy type and research review of antisocial behavior from the perspective of prediction[J]. Acad J Jinyang, 2020, 41(2): 104-114. https://www.cnki.com.cn/Article/CJFDTOTAL-JYXK202002015.htm
[2]	DUARTE C S, KLOTZ J, ELKINGTON K, et al. Severity and frequency of antisocial behaviors: late adolescence/young adulthood antisocial behavior index[J]. J Child Fam Stud, 2020, 29(12): 1200-1211. doi: 10.1007/s10826-019-01661-9
[3]	World Health Organization. Youth violence[EB/OL]. [2020-09-28]. http://www.who.int/news-room/fact-sheets/detail/youth-violence.
[4]	国家统计局. 2018年《中国儿童发展纲要(2011—2020年)》统计监测报告[EB/OL]. [2020-07-01]. http://www.stats.gov.cn/tjsj/zxfb/201912/t20191206_1715751.html. National Bureau of Statistics of the People's Republic of China. Statistical monitoring report on the program for the development of Chinese children (2011-2020) in 2018[EB/OL]. [2020-07-01]. http://www.stats.gov.cn/tjsj/zxfb/201912/t20191206_1715751.html.
[5]	GHANDOUR R M, SHERMAN L J, VLADUTIU C J, et al. Prevalence and treatment of depression, anxiety, and conduct problems in US children[J]. J Pediatr, 2019, 206: 256-267. DOI: 10.1016/j.jpeds.2018.09.021.
[6]	FAIRCHILD G, HAWES D J, FRICK P J, et al. Conduct disorder[J]. Nat Rev Dis Prim, 2019, 5(1): 43. doi: 10.1038/s41572-019-0095-y
[7]	KOELCH M G, DÖPFNER M, FREITAG C M, et al. Conduct disorder and antisocial personality disorders: challenges for treatment in adolescence and young adulthood[J]. Fortschr Neurol Psychiatr, 2019, 87(11): 634-637. doi: 10.1055/a-0984-5929
[8]	CASTILLO-EITO L, ARMITAGE C J, NORMAN P, et al. How can adolescent aggression be reduced? A multi-level meta-analysis[J]. Clin Psychol Rev, 2020, 78. DOI: 10.1016/j.cpr.2020.101853.
[9]	JIN J. Interventions to prevent child maltreatment[J]. JAMA, 2018, 320(20): 2160. doi: 10.1001/jama.2018.17741
[10]	World Health Organization. Child maltreatment[EB/OL]. [2020-09-28]. https://www.who.int/news-room/fact-sheets/detail/child-maltreatment.
[11]	KUHLMAN K R, GEISS E G, VARGAS I, et al. HPA-axis activation as a key moderation of childhood trauma exposure and adolescent mental health[J]. J Abnorm Child Psychol, 2018, 46(1): 149-157. doi: 10.1007/s10802-017-0282-9
[12]	DAHMEN B, PUETZ V B, SCHARKE W, et al. Effects of early-life adversity on hippocampal structures and associated HPA axis functions[J]. Dev Neurosci, 2018, 40(1): 13-22. doi: 10.1159/000484238
[13]	NEMEROFF C B. Paradise Lost: the neurobiological and clinical consequences of child abuse and neglect[J]. Neuron, 2016, 89(5): 892-909. doi: 10.1016/j.neuron.2016.01.019
[14]	MCCRORY E J, DE BRITO S A, KELLY P A, et al. Amygdala activation in maltreated children during pre-attentive emotional processing[J]. Br J Psychiatry, 2013, 202(4): 269-276. doi: 10.1192/bjp.bp.112.116624
[15]	SUZUKI H, LUBY J L, BOTTERON K N, et al. Early life stress and trauma and enhanced limbic activation to emotionally valenced faces in depressed and healthy children[J]. J Am Acad Child Adolesc Psychiatry, 2014, 53(7): 800-813. doi: 10.1016/j.jaac.2014.04.013
[16]	VAN HARMELEN A L, VAN TOL M J, DALGLEISH T, et al. Hypoactive medial prefrontal cortex functioning in adults reporting childhood emotional maltreatment[J]. Soc Cogn Affect Neurosci, 2014, 9(12): 2026-2033. doi: 10.1093/scan/nsu008
[17]	HYDE L W, BYRD A L, VOTRUBA-DRZAL E, et al. Amygdala reactivity and negative emotionality: divergent correlates of antisocial personality and psychopathy traits in a community sample[J]. J Abn Psychol, 2014, 123(1): 214-224. doi: 10.1037/a0035467
[18]	HYDE L W, SHAW D S, MURRAY L, et al. Dissecting the role of amygdala reactivity in antisocial behavior in a sample of young, low-income, urban men[J]. Clin Psychol Sci, 2016, 4(3): 527-544. doi: 10.1177/2167702615614511
[19]	BORTOLATO M, FLORIS G, SHIH J C. From aggression to autism: new perspectives on the behavioral sequelae of monoamine oxidase deficiency[J]. J Neural Transm (Vienna), 2018, 125(11): 1589-1599. doi: 10.1007/s00702-018-1888-y
[20]	GODAR S C, FITE P J, MCFARLIN K M, et al. The role of monoamine oxidase A in aggression: current translational developments and future challenges[J]. Prog Neuropsychopharmacol Biol Psychiatry, 2016, 69: 90-100. DOI: 10.1016/j.pnpbp.2016.01.001.
[21]	SABOL S Z, HU S, HAMER D. A functional polymorphism in the monoamine oxidase A gene promoter[J]. Hum Genet, 1998, 103(3): 273-279. doi: 10.1007/s004390050816
[22]	RODRIGUEZ-RAMOS A, MORIANA J A, GARCIA-TORRES F, et al. Emotional stability is associated with the MAOA promoter uVNTR polymorphism in women[J]. Brain Behav, 2019, 9(9): e1376. doi: 10.1002/brb3.1376
[23]	GUO G, OU X M, ROETTGER M, et al. The VNTR 2 repeat in MAOA and delinquent behavior in adolescence and young adulthood: associations and MAOA promoter activity[J]. Eur J Hum Genet, 2008, 16(5): 626-634. doi: 10.1038/sj.ejhg.5201999
[24]	HUANG Y Y, CATE S P, BATTISTUZZI C, et al. An association between a functional polymorphism in the monoamine oxidase a gene promoter, impulsive traits and early abuse experiences[J]. Neuropsychopharmacology, 2004, 29(8): 1498-1505. doi: 10.1038/sj.npp.1300455
[25]	BEACH S R H, BRODY G H, GUNTER T D, et al. Child maltreatment moderates the association of MAOA with symptoms of depression and antisocial personality disorder[J]. J Fam Psychol, 2010, 24(1): 12-20. doi: 10.1037/a0018074
[26]	GODAR S C, FITE P J, MCFARLIN K M, et al. The role of monoamine oxidase A in aggression: current translational developments and future challenges[J]. Pro Neuropsychopharmacol Biol Psychiatry, 2016, 69: 90-100. DOI: 10.1016/j.pnpbp.2016.01.001.
[27]	BORTOLATO M, GODAR S C, TAMBARO S, et al. Early postnatal inhibition of serotonin synthesis results in long-term reductions of preservative behaviors, but not aggression, in MAO A-deficient mice[J]. Neuropharmacology, 2013, 75: 223-232. DOI: 10.1016/j.neuropharm.2013.07.003.
[28]	GALUPA R, HEARD E. X-chromosome inactivation: a crossroads between chromosome architecture and gene regulation[J]. Annu Rev Genet, 2018, 52: 535-566. DOI: 10.1146/annurev-genet-120116-024611.
[29]	CASPI A, MCCLAY J, MOFFITT T E, et al. Role of genotype in the cycle of violence in maltreated children[J]. Science, 2002, 297(5582): 851-854. doi: 10.1126/science.1072290
[30]	NEWMAN T K, SYAGAILO Y V, BARR C S, et al. Monoamine oxidase a gene promoter variation and rearing experience influences aggressive behavior in rhesus monkeys[J]. Biol Psychiatry, 2005, 57(2): 167-172. doi: 10.1016/j.biopsych.2004.10.012
[31]	KARERE G M, KINNALLY E L, SANCHEZ J N, et al. What is an "adverse" environment? Interactions of rearing experiences and MAOA genotype in rhesus monkeys[J]. Biol Psychiatry, 2009, 65(9): 770-777. doi: 10.1016/j.biopsych.2008.11.004
[32]	CHOE D E, SHAW D S, HYDE L W, et al. Interactions between monoamine oxidase a and punitive discipline in African American and Caucasian men's antisocial behavior[J]. Clin Psychol Sci, 2014, 2(5): 591-601. doi: 10.1177/2167702613518046
[33]	NILSSON K W, COMASCO E, HODGINS S, et al. Genotypes do not confer risk for delinquency but rather alter susceptibility to positive and negative environmental factors: gene-environmentinteractions of BDNF Val66Met, 5-HTTLPR, and MAOA-uVNTR[J]. Int J Neuropsychopharmacol, 2014, 18(5): 107. http://ijnp.oxfordjournals.org/content/18/5/pyu107
[34]	ZHANG Y, MING Q, WANG X, et al. The interactive effect of the MAOA-VNTR genotype and childhood abuse on aggressive behaviors in Chinese male adolescents[J]. Psychiatr Genet, 2016, 26(3): 117-123. doi: 10.1097/YPG.0000000000000125
[35]	MCGRATH M L, MUSTANSKI B, METZGER A, et al. A latent modeling approach to genotype-phenotype relationships: maternal problem behavior clusters, prenatal smoking, and MAOA genotype[J]. Arch Womens Ment Health, 2012, 15(4): 269-282. doi: 10.1007/s00737-012-0286-y
[36]	EISNER P, KLASEN M, WOLF D, et al. Cortico-limbic connectivity in MAOA-L carriers is vulnerable to acute tryptophan depletion[J]. Hum Brain Mapp, 2017, 38(3): 1622-1635. doi: 10.1002/hbm.23475
[37]	TEICHER M H, ANDERSEN S L, POLCARI A, et al. The neurobiological consequences of early stress and childhood maltreatment[J]. Neurosci Biobehav Rev, 2003, 27(1/2): 33-44. http://www.sciencedirect.com/science/article/pii/S0149763403000071
[38]	TOTTENHAM N. The importance of early experiences for neuro-affective development[J]. Curr Top Behav Neurosci, 2014, 16: 109-129. DOI: 10.1007/7854_2013_254.
[39]	WILLIAMS L M, GATT J M, KUAN S A, et al. A polymorphism of the MAOA gene is associated with emotional brain markers and personality traits on an antisocial index[J]. Neuropsychopharmacology, 2009, 34(7): 1797-1809. doi: 10.1038/npp.2009.1
[40]	BYRD A L, MANUCK S B, HAWES S W, et al. The interaction between monoamine oxidase A (MAOA) and childhood maltreatment as a predictor of personality pathology in females: Emotional reactivity as a potential mediating mechanism[J]. Dev Psychopathol, 2018: 1-17. DOI: 10.1017/s0954579418000238.
[41]	CASEY B J, HELLER A S, GEE D G, et al. Development of the emotional brain[J]. Neurosci Lett, 2019, 693: 29-34. DOI: 10.1016/j.neulet.2017.11.055.
[42]	LATHAM M D, COOK N, SIMMONS J G, et al. Physiological correlates of emotional reactivity and regulation in early adolescents[J]. Biol Psychol, 2017, 127: 229-238. DOI: 10.1016/j.biopsycho.2017.07.018.
[43]	MEYER-LINDENBERG A, BUCKHOLTZ J W, KOLACHANA B, et al. Neural mechanisms of genetic risk for impulsivity and violence in humans[J]. Proc Natl Acad Sci USA, 2006, 103(16): 6269-6274. doi: 10.1073/pnas.0511311103
[44]	HOLZ N, BOECKER R, BUCHMANN A F, et al. Evidence for a sex-dependent MAOA×childhood stress interaction in the Neural circuitry of aggression[J]. Cereb Cortex, 2016, 26(3): 904-914. doi: 10.1093/cercor/bhu249
[45]	KOLLA N J, VINETTE S A. Monoamine oxidase A in antisocial personality disorder and borderline personality disorder[J]. Curr Behav Neurosci Rep, 2017, 4(1): 41-48. doi: 10.1007/s40473-017-0102-0
[46]	KONAR A, RASTOGI M, BHAMBRI A. Brain region specific methylation and Sirt1 binding changes in MAOA promoter is associated with sexual dimorphism in early life stress induced aggressive behavior[J]. Neurochem Int, 2019, 129: 104510. DOI: 10.1016/j.neuint.2019.104510.
[47]	WAGELS L, VOTINOV M, KELLERMANN T, et al. Exogenous testosterone and the monoamine-oxidase A polymorphism influence anger, aggression and neural responses to provocation in males[J]. Neuropharmacology, 2019, 156: 107491. DOI: 10.1016/j.neuropharm.2019.01.006.
[48]	RUISCH I H, DIETRICH A, GLENNON J C, et al. Interplay between genome-wide implicated genetic variants and environmental factors related to childhood antisocial behavior in the UK ALSPAC cohort[J]. Eur Arch Psychiatry Clin Neurosci, 2019, 269(6): 741-752. doi: 10.1007/s00406-018-0964-5
[49]	ZHANG Y, MING Q, YI J, et al. Gene-gene-environment interactions of serotonin transporter, monoamine oxidase a and childhood maltreatment predict aggressive behavior in Chinese adolescents[J]. Front Behav Neurosci, 2017, 11: 17. DOI: 10.3389/fnbeh.2017.00.017.
[50]	OUELLET-MORIN I, COTE S M, VITARO F, et al. Effects of the MAOA gene and levels of exposure to violence on antisocial outcomes[J]. Br J Psychiatry, 2016, 208(1): 42-48. doi: 10.1192/bjp.bp.114.162081
[51]	NILSSON K W, ÅSLUND C, COMASCO E, et al. Gene-environment interaction of monoamine oxidase A in relation to antisocial behaviour: current and future directions[J]. J Neural Transm, 2018, 125(11): 1601-1626. doi: 10.1007/s00702-018-1892-2
[52]	CHECKNITA D, BENDRE M, EKSTRÖM T J, et al. Monoamine oxidase A genotype and methylation moderate the association of maltreatment and aggressive behaviour[J]. Behav Brain Res, 2020, 382: 112476. DOI: 10.1016/j.bbr.2020.112476.