Genetic bases of attention deficit hyperactivity disorder

被引:12
作者
Sanchez-Mora, Cristina [1 ]
Ribases, Marta [1 ]
Mulas, Fernando [3 ]
Soutullo, Cesar [4 ]
Sans, Anna [5 ]
Pamias, Montserrat [6 ,7 ]
Casas, Miguel [8 ]
Antoni Ramos-Quiroga, Josep [2 ,8 ]
机构
[1] Vall Hebron Inst Recerca, Lab Psiquiatria Genet, Barcelona, Spain
[2] Hosp Univ Vall dHebron, Serv Psiquiatria, CIBERSAM, E-08035 Barcelona, Spain
[3] INVANEP, Inst Valenciano Neurol Pediat, Valencia, Spain
[4] Univ Navarra, Fac Med, Clin Univ, Dept Psiquiatria & Psicol Med,Unidad Psiquiatria, Navarra, Spain
[5] Hosp St Joan de Deu, Serv Neurol, UTAE, Unidad Trastornos Aprendizaje, Barcelona, Spain
[6] Corp Sanitaria, Serv Salud Mental, Area Psiquiatria Infantil, Barcelona, Spain
[7] Univ Parc Tauli, Barcelona, Spain
[8] Univ Autonoma Barcelona, Fac Med, Dept Psiquiatria & Med Legal, E-08193 Barcelona, Spain
关键词
ADHD; ADRA2A; CES1; COMT; DAT1; DRD4; Genetics; LPHN3; OPRM1; DOPAMINE-D4 RECEPTOR GENE; SEROTONIN TRANSPORTER GENE; FAMILY-BASED ASSOCIATION; DEFICIT/HYPERACTIVITY DISORDER; CANDIDATE GENE; ADULT ADHD; METHYLPHENIDATE RESPONSE; ADRENERGIC-RECEPTOR; POPULATION-SAMPLE; PATIENTS SUGGEST;
D O I
10.33588/rn.5510.2012344
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Aims. The purpose of this study is to update the information available on the main group of genes that have been related with a susceptibility to attention deficit hyperactivity disorder (ADHD) or with the pharmacological response to different drugs used in the treatment of ADHD, in a number of different association and meta-analysis studies. Development. Different studies have provided evidence of the importance of the genetic load in the susceptibility to ADHD. The work carried out to date point to genes in the dopaminergic system, such as the gene that codes for the dopamine transporter (DAT1 or SLC6A3) and for the dopamine receptor D-4 (DRD4); in the noradrenergic system, like the gene coding for the adrenergic alpha-2A receptor (ADRA2A), the COMT gene, which codes for the enzyme catechol-O-methyltransferase and the gene that codes for latrophilin 3 (LPHN3), as genes that are candidates for playing a part in the susceptibility to ADHD, and being involved in the pharmacological response as well as in the risk of presenting associated behavioural disorders. On the other hand, the genes involved in regulating the metabolism of the drugs used in the treatment of ADHD, such as the gene CYP2D6 and gene CES1, play a role in the efficiency and tolerance of these psycho-pharmaceuticals. Conclusions. Although in recent years there has been an increase in the number of pharmacogenetic studies conducted on ADHD, findings differ significantly from one study to another. Integrating and meta-analytical studies are needed to be able to develop a more personalised treatment for ADHD.
引用
收藏
页码:609 / 618
页数:10
相关论文
共 106 条
  • [1] Methylphenidate increases cortical excitability via activation of alpha-2 noradrenergic receptors
    Andrews, GD
    Lavin, A
    [J]. NEUROPSYCHOPHARMACOLOGY, 2006, 31 (03) : 594 - 601
  • [2] Parent of Origin Effects in Attention/Deficit Hyperactivity Disorder (ADHD): Analysis of Data From the International Multicenter ADHD Genetics (IMAGE) Program
    Anney, Richard J. L.
    Hawi, Ziarih
    Sheehan, Karen
    Mulligan, Aisling
    Pinto, Carlos
    Brookes, Keeley J.
    Xu, Xiaohui
    Zhou, Kaixin
    Franke, Barbara
    Buitelaar, Jan
    Vermeulen, Sita H.
    Banaschewski, Tobias
    Sonuga-Barke, Edmund J. S.
    Ebstein, Richard
    Manor, Iris
    Miranda, Ana
    Mulas, Fernando
    Oades, Robert D.
    Roeyers, Herbert
    Rommelse, Nanda
    Rothenberger, Aribert
    Sergeant, Joseph
    Steinhausen, Hans-Christoph
    Taylor, Eric
    Thompson, Margaret
    Asherson, Philip
    Faraone, Stephen V.
    Gill, Michael
    [J]. AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS, 2008, 147B (08) : 1495 - 1500
  • [3] Aragonès E, 2010, REV ESP SALUD PUBLIC, V84, P417
  • [4] A common variant of the latrophilin 3 gene, LPHN3, confers susceptibility to ADHD and predicts effectiveness of stimulant medication
    Arcos-Burgos, M.
    Jain, M.
    Acosta, M. T.
    Shively, S.
    Stanescu, H.
    Wallis, D.
    Domene, S.
    Velez, J. I.
    Karkera, J. D.
    Balog, J.
    Berg, K.
    Kleta, R.
    Gahl, W. A.
    Roessler, E.
    Long, R.
    Lie, J.
    Pineda, D.
    Londono, A. C.
    Palacio, J. D.
    Arbelaez, A.
    Lopera, F.
    Elia, J.
    Hakonarson, H.
    Johansson, S.
    Knappskog, P. M.
    Haavik, J.
    Ribases, M.
    Cormand, B.
    Bayes, M.
    Casas, M.
    Ramos-Quiroga, J. A.
    Hervas, A.
    Maher, B. S.
    Faraone, S. V.
    Seitz, C.
    Freitag, C. M.
    Palmason, H.
    Meyer, J.
    Romanos, M.
    Walitza, S.
    Hemminger, U.
    Warnke, A.
    Romanos, J.
    Renner, T.
    Jacob, C.
    Lesch, K-P
    Swanson, J.
    Vortmeyer, A.
    Bailey-Wilson, J. E.
    Castellanos, F. X.
    [J]. MOLECULAR PSYCHIATRY, 2010, 15 (11) : 1053 - 1066
  • [5] Toward a better understanding of ADHD: LPHN3 gene variants and the susceptibility to develop ADHD
    Arcos-Burgos, Mauricio
    Muenke, Maximilian
    [J]. ADHD-ATTENTION DEFICIT AND HYPERACTIVITY DISORDERS, 2010, 2 (03) : 139 - 147
  • [6] Identification of DNA variants in the SNAP-25 gene and linkage study of these polymorphisms and attention-deficit hyperactivity disorder
    Barr, CL
    Feng, Y
    Wigg, K
    Bloom, S
    Roberts, W
    Malone, M
    Schachar, R
    Tannock, R
    Kennedy, JL
    [J]. MOLECULAR PSYCHIATRY, 2000, 5 (04) : 405 - 409
  • [7] Barr CL, 2001, AM J MED GENET, V105, P84, DOI 10.1002/1096-8628(20010108)105:1<84::AID-AJMG1068>3.0.CO
  • [8] 2-Q
  • [9] Absence of 5-HT1B receptors is associated with impaired impulse control in male 5-HT1B knockout mice
    Bouwknecht, JA
    Hijzen, TH
    van der Gugten, J
    Mass, RAA
    Hen, R
    Olivier, B
    [J]. BIOLOGICAL PSYCHIATRY, 2001, 49 (07) : 557 - 568
  • [10] The analysis of 51 genes in DSM-IV combined type attention deficit hyperactivity disorder:: association signals in DRD4, DAT1 and 16 other genes
    Brookes, K.
    Xu, X.
    Chen, W.
    Zhou, K.
    Neale, B.
    Lowe, N.
    Aneey, R.
    Franke, B.
    Gill, M.
    Ebstein, R.
    Buitelaar, J.
    Sham, P.
    Campbell, D.
    Knight, J.
    Andreou, P.
    Altink, M.
    Arnold, R.
    Boer, F.
    Buschgens, C.
    Butler, L.
    Christiansen, H.
    Feldman, L.
    Fleischman, K.
    Fliers, E.
    Howe-Forbes, R.
    Goldfarb, A.
    Heise, A.
    Gabriels, I.
    Korn-Lubetzki, I.
    Marco, R.
    Medad, S.
    Minderaa, R.
    Mulas, F.
    Mueller, U.
    Mulligan, A.
    Rabin, K.
    Rommelse, N.
    Sethna, V.
    Sorohan, J.
    Uebel, H.
    Psychogiou, L.
    Weeks, A.
    Barrett, R.
    Craig, I.
    Banaschewski, T.
    Sonuga-Barke, E. J. S.
    Eisenberg, J.
    Kuntsi, J.
    Manor, I.
    McGuffin, P.
    [J]. MOLECULAR PSYCHIATRY, 2006, 11 (10) : 934 - 953