Association between genetic variation of ionized glutamate receptors and attention deficit hyperactivity disorder

XIONG Ping, ZHU Hongmin, HUANG Xin, WU Jing, LIN Jing, ZHONG Yanyan

Chinese Journal of Child Health Care ›› 2023, Vol. 31 ›› Issue (9) : 945-950.

PDF(580 KB)
PDF(580 KB)
Chinese Journal of Child Health Care ›› 2023, Vol. 31 ›› Issue (9) : 945-950. DOI: 10.11852/zgetbjzz2022-1372
Original Articles

Association between genetic variation of ionized glutamate receptors and attention deficit hyperactivity disorder

  • XIONG Ping1, ZHU Hongmin1, HUANG Xin2, WU Jing2, LIN Jing3, ZHONG Yanyan3
Author information +
History +

Abstract

Objective To analyze the association between genetic variation of ionized glutamate receptors (iGluRs) and attention deficit hyperactivity disorder (ADHD), so as to provide a theoretical basis for elucidating the pathogenesis of ADHD. Methods A case-control study was conducted for the potential candidate genes of ADHD, including GRIN2A, GRIN2B, GRIK1, GRIK4 and GRID2. A total of 320 ADHD children were recruited as the ADHD group in Wuhan Children's Hospital from August 2018 to December 2019, meanwhile 355 typically developed children were enrolled in the control group. All children were evaluated by Conners Parental Syndrome Questionnaire (PSQ). The associations of a single site with the risk of ADHDand ADHD symptoms were examined. Results There were no significant differences in age, sex ratio and intelligence quotient between the ADHD and control groups (P>0.05). The TT genotype frequency of rs1385405 locus on GRID2 gene showed a significant difference between the two groups (P=0.001). Individuals carrying the TT genotype at this locus were 2.725 times more likely to develop ADHD than those carrying the GG genotype (OR=2.725). In the ADHD-C subtype, there was a significant difference between the genotype frequency of this polymorphic locus (P=0.004). The risk of ADHD-C in individuals carrying TT genotype was 2.343 times as high as that in individuals carrying GG genotype (OR=2.343). In addition, there was an association between this locus and ADHD symptoms, with a significant difference in total PSQ scores among individuals carrying different genotypes (F=6.711, P=0.001). Conclusion GRID2-rs1385405 is associated with the susceptibility of ADHD in Chinese Han children, and TT genotype is a risk factor.

Key words

ionic glutamate receptor / attention deficit hyperactivity disorder / heredity / gene

Cite this article

Download Citations
XIONG Ping, ZHU Hongmin, HUANG Xin, WU Jing, LIN Jing, ZHONG Yanyan. Association between genetic variation of ionized glutamate receptors and attention deficit hyperactivity disorder[J]. Chinese Journal of Child Health Care. 2023, 31(9): 945-950 https://doi.org/10.11852/zgetbjzz2022-1372

References

[1] Posner J,Polanczyk GV, Sonuga-Barke E. Attention-deficit hyperactivity disorder[J]. Lancet, 2020,395(10222):450-462.
[2] Faraone SV, Larsson H. Genetics of attention deficit hyperactivity disorder[J]. Mol Psychiatry, 2019,24(4):562-575.
[3] Faraone SV, Perlis RH, Doyle AE, et al. Molecular genetics of attention-deficit/hyperactivity disorder[J]. Biol Psychiatry, 2005,57(11):1313-1323.
[4] Naaijen J, Bralten J, Poelmans G, et al. Glutamatergic and GABAergic gene sets in attention-deficit/hyperactivity disorder:Association to overlapping traits in ADHD and autism[J]. Transl Psychiatry, 2017,7(1):e999.
[5] Hinney A, Scherag A, Jarick I, et al. Genome-wide association study in German patients with attention deficit/hyperactivity disorder[J]. Am J Med Genet B Neuropsychiatr Genet, 2011,156B(8):888-897.
[6] Lasky-Su J, Neale BM, Franke B, et al. Genome-wide association scan of quantitative traits for attention deficit hyperactivity disorder identifies novel associations and confirms candidate gene associations[J]. Am J Med Genet B Neuropsychiatr Genet, 2008,147B(8):1345-1354.
[7] American Psychiatric Association. Diagnostic and statistical manual of mental disorders[M].4th ed. Arlington, VA, 1994.
[8] Kieng S, Rossier J, Favez N, et al. Long-term stability of the French WISC-Ⅳ: Standard and CHC index scores[J]. Eur Rev Appl Psychol, 2017, 67:51-60.
[9] Zhang HC. The Revision of WISC-Ⅳ Chinese Version[J]. Psychological Science, 2009, 32:1177-1179.
[10] Conners CK, Pitkanen J, Rzepa SR. Conners comprehensive behavior rating scale[M]// Kreutzer JS, DeLuca J, Caplan B. Encyclopedia of clinical neuropsychology. Berlin: Springer, 2011.
[11] 范娟,杜亚松,王立伟.Conners父母用症状问卷的中国城市常模和信度研究[J].上海精神医学,2005,17(6):321-323.
Fan J,Du YS,Wang LW.The norm and reliability of the Conners Parent Symptom Questionnaire in Chinese urban children[J].Shanghai Archives of Psychiatry,2005,17(6):321-323.(in Chinese)
[12] Yelshanskaya MV, Li M, Sobolevsky AI. Structure of an agonist-bound ionotropic glutamate receptor[J]. Science, 2014,345(6200):1070-1074.
[13] Traynelis SF, Wollmuth LP, McBain CJ, et al. Glutamate receptor ion channels:Structure, regulation, and function[J].Pharmacol Rev, 2010,62(3):405-496.
[14] Zhang Q, Huang X, Chen XZ,, et al. Association of gene variations in ionotropic glutamate receptor and attention-deficit/hyperactivity disorder in the Chinese population: A two-stage case-control study[J]. J Atten Disord, 2021, 25(10):1362-1373.
[15] Turic D, Langley K, Mills S, et al. Follow-up of genetic linkage findings on chromosome 16p13:Evidence of association of N-methyl-D aspartate glutamate receptor 2A gene polymorphism with ADHD[J]. Mol Psychiatry, 2004,9(2):169-173.
[16] Park S, Jung SW, Kim BN, et al. Association between the GRM7 rs3792452 polymorphism and attention deficithyperacitiveity disorder in a Korean sample[J]. Behav Brain Funct, 2013, 9(1):1.doi:org/10.1186/1744-9081-9-1
[17] Kim JI, Kim JW, Park JE, et al. Association of the GRIN2B rs2284411 polymorphism with methylphenidate response in attention-deficit/hyperactivity disorder[J]. J Psychopharmacol, 2017,31(8):1070-1077.
[18] Stergiakouli E, Hamshere M, Holmans P, et al. Investigating the contribution of common genetic variants to the risk and pathogenesis of ADHD[J]. Am J Psychiatry, 2012,169(2):186-194.
[19] Araki K, Meguro H,Kushiya E, et al. Selective expression of the glutamate receptor channel delta 2 subunit in cerebellar Purkinje cells[J]. Biochem Biophys Res Commun, 1993,197(3):1267-1276.
[20] Demontis D, Walters RK, Martin J, et al. Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder[J]. Nat Genet, 2019,51(1):63-75.
[21] Gazzellone MJ, Zhou X, Lionel AC, et al. Copy number variation in Han Chinese individuals with autism spectrum disorder[J]. J Neurodev Disord, 2014, 6(1):34.
[22] Pinto D,Delaby E, Merico D, et al. Convergence of genes and cellular pathways dysregulated in autism spectrum disorders[J]. Am J Hum Genet, 2014, 94(5):677-694.
[23] Thompson JA,Ziman M. Pax genes during neural development and their potential role in neuroregeneration[J]. Prog Neurobiol, 2011, 95(3):334-351.
[24] Hoogman M, Muetzel R, Guimaraes JP, et al. Brain imaging of the cortex in ADHD: A coordinated analysis of large-scale clinical and population-based samples[J]. Am J Psychiatry, 2019,176(7):531-542.
PDF(580 KB)

Accesses

Citation

Detail

Sections
Recommended

/