Race Moderates the Association of Catechol-O-methyltransferase Genotype and Posttraumatic Stress Disorder in Preschool Children

被引:13
作者
Humphreys, Kathryn L. [1 ]
Scheeringa, Michael S. [1 ]
Drury, Stacy S. [1 ]
机构
[1] Tulane Univ, Sch Med, New Orleans, LA 70112 USA
关键词
DOPAMINE TRANSPORTER; PTSD; GENE; BRAIN; COMT;
D O I
10.1089/cap.2014.0077
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Objective: The present study sought to replicate previous findings of an association between the Catechol-O-methyltransferase (COMT) val158met polymorphism with posttraumatic stress disorder (PTSD) and symptomatology in a novel age group, preschool children. Methods:COMT genotype was determined in a sample of 171 3-6-year-old trauma-exposed children. PTSD was assessed with a semistructured interview. Accounting for sex, trauma type, and age, genotype was examined in relation to categorical and continuous measures of PTSD both controlling for race and within the two largest racial categories (African American [AA] and European American [EA]). Results: Race significantly moderated the association between genotype and PTSD. Specifically, the genotype associated with increased PTSD symptoms in one racial group had the opposite association in the other racial group. For AA children the met/met genotype was associated with more PTSD symptoms. However, for EA children, val allele carriers had more PTSD symptoms. Whereas every AA child with the met/met genotype met criteria for PTSD, none of the EA children with the met/met genotype did. This genetic association with COMT genotype, in both races but in opposite directions, was most associated with increased arousal symptoms. Conclusions: These findings replicate previous findings in participants of African descent, highlight the moderating effect of race on the association between COMT genotype and PTSD, and provide direct evidence that consideration of population stratification within gene-by-environment studies is valuable to prevent false negative findings.
引用
收藏
页码:454 / 457
页数:4
相关论文
共 17 条
[1]  
Berg K, 2005, AM J HUM GENET, V77, P519
[2]   Higher FKBP5, COMT, CHRNA5, and CRHR1 allele burdens are associated with PTSD and interact with trauma exposure: implications for neuropsychiatric research and treatment [J].
Boscarino, Joseph A. ;
Erlich, Porat M. ;
Hoffman, Stuart N. ;
Zhang, Xiaopeng .
NEUROPSYCHIATRIC DISEASE AND TREATMENT, 2012, 8 :131-139
[3]   Population stratification and spurious allelic association [J].
Cardon, LR ;
Palmer, LJ .
LANCET, 2003, 361 (9357) :598-604
[4]  
Chang SC, 2012, PLOS ONE, V7
[5]   Functional analysis of genetic variation in catechol-o-methyltransferase (COMT):: Effects on mRNA, protein, and enzyme activity in postmortem human brain [J].
Chen, JS ;
Lipska, BK ;
Halim, N ;
Ma, QD ;
Matsumoto, M ;
Melhem, S ;
Kolachana, BS ;
Hyde, TM ;
Herman, MM ;
Apud, J ;
Egan, MF ;
Kleinman, JE ;
Weinberger, DR .
AMERICAN JOURNAL OF HUMAN GENETICS, 2004, 75 (05) :807-821
[6]   The Association of a Novel Haplotype in the Dopamine Transporter with Preschool Age Posttraumatic Stress Disorder [J].
Drury, Stacy S. ;
Brett, Zoe H. ;
Henry, Caitlin ;
Scheeringa, Michael .
JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY, 2013, 23 (04) :236-243
[7]   The Role of the Dopamine Transporter (DAT) in the Development of PTSD in Preschool Children [J].
Drury, Stacy S. ;
Theall, Katherine P. ;
Keats, Bronya J. B. ;
Scheeringa, Michael .
JOURNAL OF TRAUMATIC STRESS, 2009, 22 (06) :534-539
[8]   CHROMOSOMAL MAPPING OF THE HUMAN CATECHOL-O-METHYLTRANSFERASE GENE TO 22Q11.1-]Q11.2 [J].
GROSSMAN, MH ;
EMANUEL, BS ;
BUDARF, ML .
GENOMICS, 1992, 12 (04) :822-825
[9]   Replication validity of genetic association studies [J].
Ioannidis, JPA ;
Ntzani, EE ;
Trikalinos, TA ;
Contopoulos-Ioannidis, DG .
NATURE GENETICS, 2001, 29 (03) :306-309
[10]   The Risk of Posttraumatic Stress Disorder After Trauma Depends on Traumatic Load and the Catechol-O-Methyltransferase Val158Met Polymorphism [J].
Kolassa, Iris-Tatjana ;
Kolassa, Stephan ;
Ertl, Verena ;
Papassotiropoulos, Andreas ;
De Quervain, Dominique J. -F. .
BIOLOGICAL PSYCHIATRY, 2010, 67 (04) :304-308