Research output: Contribution to journal › Article
Rare DNA variants in the brain derived neurotrophic factor gene increase risk for attention deficit hyperactivity disorder : a next generation sequencing study. / Hawi, Ziarih; Cummins, Tarrant D R; Tong, Janette; Arcos-Burgos, Mauricio; Zhao, Qiongyi; Matthews, Natasha; Newman, Daniel P; Johnson, Beth; Vance, Alasdair; Heussler, Helen S; Levy, Florence; Easteal, Simon; Wray, Naomi; Kenny, Elaine; Morris, Derek; Kent, Lindsey; Gill, Michael; Bellgrove, Mark.
In: Molecular Psychiatry, Vol. 22, No. 4, 04.2017, p. 580-584.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Rare DNA variants in the brain derived neurotrophic factor gene increase risk for attention deficit hyperactivity disorder
T2 - a next generation sequencing study
AU - Hawi, Ziarih
AU - Cummins, Tarrant D R
AU - Tong, Janette
AU - Arcos-Burgos, Mauricio
AU - Zhao, Qiongyi
AU - Matthews, Natasha
AU - Newman, Daniel P
AU - Johnson, Beth
AU - Vance, Alasdair
AU - Heussler, Helen S
AU - Levy, Florence
AU - Easteal, Simon
AU - Wray, Naomi
AU - Kenny, Elaine
AU - Morris, Derek
AU - Kent, Lindsey
AU - Gill, Michael
AU - Bellgrove, Mark
N1 - This work was supported by a grant from the National Health and Medical Research Council of Australia (NHMRC) (APP1065677).
PY - 2017/4
Y1 - 2017/4
N2 - Attention deficit hyperactivity disorder (ADHD) is a prevalent and highly heritable disorder of childhood with negative lifetime outcomes. Although candidate gene and genome wide association studies have identified promising common variant signals, these explain only a fraction of the heritability of ADHD. The observation that rare structural variants confer substantial risk to psychiatric disorders suggests that rare variants might explain a portion of the missing heritability for ADHD. Here we performed the first large-scale next generation targeted sequencing study of ADHD in 152 child and adolescent cases and 188 controls across an a priori set of 117 genes. A multi-marker gene level analysis of rare (< 1% frequency) single nucleotide variants (SNVs) revealed that the gene encoding brain derived neurotrophic factor (BDNF) was associated with ADHD at Bonferroni corrected levels. Sanger sequencing confirmed the existence of all novel rare BDNF variants. Our results implicate BDNF as a genetic risk factor for ADHD, potentially by virtue of its critical role in neurodevelopment and synaptic plasticity.
AB - Attention deficit hyperactivity disorder (ADHD) is a prevalent and highly heritable disorder of childhood with negative lifetime outcomes. Although candidate gene and genome wide association studies have identified promising common variant signals, these explain only a fraction of the heritability of ADHD. The observation that rare structural variants confer substantial risk to psychiatric disorders suggests that rare variants might explain a portion of the missing heritability for ADHD. Here we performed the first large-scale next generation targeted sequencing study of ADHD in 152 child and adolescent cases and 188 controls across an a priori set of 117 genes. A multi-marker gene level analysis of rare (< 1% frequency) single nucleotide variants (SNVs) revealed that the gene encoding brain derived neurotrophic factor (BDNF) was associated with ADHD at Bonferroni corrected levels. Sanger sequencing confirmed the existence of all novel rare BDNF variants. Our results implicate BDNF as a genetic risk factor for ADHD, potentially by virtue of its critical role in neurodevelopment and synaptic plasticity.
U2 - 10.1038/mp.2016.117
DO - 10.1038/mp.2016.117
M3 - Article
VL - 22
SP - 580
EP - 584
JO - Molecular Psychiatry
JF - Molecular Psychiatry
SN - 1359-4184
IS - 4
ER -
Research output: Contribution to journal › Article
Research output: Contribution to journal › Article
Research output: Contribution to journal › Article
Research output: Contribution to journal › Article
Research output: Contribution to journal › Article
Research output: Contribution to journal › Article
Research output: Contribution to journal › Article
Research output: Contribution to journal › Article
Research output: Contribution to journal › Article
ID: 242397596