SHORT REPORTOpen Access
Investigation of the ZNF804A gene polymorphism
with genetic risk for bipolar disorder in attention
deficit hyperactivity disorder
Xiaohui Xu1*, Gerome Breen1, Lucy Luo2, Bo Sun2, Chih-Ken Chen3,4,5, Ursula M Paredes1, Yu-Shu Huang4,5,
Yu-Yu Wu4,5and Philip Asherson1
Background: Genome-wide association studies (GWAS) have been conducted on many psychiatric disorders.
Evidence from large GWAS indicates that the single nucleotide polymorphism (SNP) rs1344706 in the zinc-finger
protein 804A gene (ZNF804A) is associated with psychotic disorders including bipolar disorder and schizophrenia.
One study also found significant association between rs1344706 and the executive control network of attention. In
this study we examine the role of the rs1344706 polymorphism that previously showed association with BD and is
known to alter expression of the gene in two clinical family-based ADHD samples from the UK and Taiwan.
Findings: To investigate the association between rs1344706 and ADHD, two family samples of ADHD probands
from the United Kingdom (n =180) and Taiwan (n =212) were genotyped using TaqMan SNP genotyping assays
and analysed using within-family transmission disequilibrium test. No significant associations were found between
rs1344706 polymorphism and ADHD in either of the samples from Taiwan (P = 0.91) and UK (P =0.41). Even
combining the two datasets together the A allele of rs1344706 SNP was still not significantly over-transmitted to
affected probands (P = 0.50). Furthermore, there was no evidence of association with the specific symptoms
subgroups of inattention or hyperactivity-impulsivity.
Conclusions: In this study we used family-based ADHD data in the UK and Taiwanese population to test for an
association between rs1344706 SNP in the ZNF804A gene and ADHD. Results showed no significant association of
rs1344706 with ADHD in UK and Taiwanese samples.
Keywords: Attention deficit hyperactivity disorder, ZNF804A, Single nucleotide polymorphism, Association study,
Attention deficit hyperactivity disorder (ADHD) is one
of the most frequent and heritable neurodevelopmental
disorders of childhood characterised by developmentally
inappropriate and impairing levels of inattention, hyper-
activity and impulsivity. Current estimates show that
3%–5% of school age children have a diagnosis of ADHD
. The disorder persists into adulthood in around two-
thirds of cases . ADHD has been associated with a
number of psychiatric comorbidities, including major
depressive disorder (MDD), bipolar disorder (BD) and
anxiety disorder [3-5]. In particular ADHD and BD
present with some overlapping clinical characteristics
and diagnostic criteria. Several studies have reported
the occurrence of high rates of emotional lability and
increased rates of depression in both child and adults
patients with ADHD [6-10]. The evidence relating to BD
and its potential link with ADHD has been reviewed
extensively [5,6] and points to a significant link with evi-
dence from clinical, epidemiological, family and neuroi-
maging studies. Review of clinical and epidemiological
studies found that the increased rate of comorbidity
between ADHD and bipolar disorder may be greater
* Correspondence: firstname.lastname@example.org
1MRC Social, Genetic and Developmental Psychiatry Centre, Institute of
Psychiatry, King’s College London, London, UK
Full list of author information is available at the end of the article
© 2013 Xu et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly cited.
Xu et al. BMC Research Notes 2013, 6:29
than that seen with other psychiatric comorbidities of
ADHD . Findings from studies of children with
ADHD suggested that combined subtype of ADHD may
be at particularly higher risk of developing BD [6,11].
A wide variety of candidate genes have been inves-
tigated in ADHD and other psychiatric disorders
including BD, with some genes reported to be asso-
ciated with both ADHD and BD [12-16]. For ex-
ample, a recent findings support the hypothesis that
variation within circadian clock genes contribute to
BD and related illnesses like ADHD, MDD and
schizophrenia, there are now several papers showing
that rare copy number variants affecting some genes
are associated with both ADHD and schizophrenia
(SZ) [18-20]. The biological mechanisms that under-
lie these shared genetic influences remain uncertain,
but could be related to common neurodevelopmental
processes, or aberrations of neurotransmitter systems
such as dopamine.
GWAS studies on ADHD have yet to identify SNPs
associations with genome-wide significance . How-
ever, promising findings from GWAS have emerged for
other psychiatric disorders, particularly SZ and BD.
GWAS identified strong evidence for association of the
zinc finger protein 804A (ZNF804A) gene (located on
the long arm of chromosome 2 at the 2q32.1) with
psychiatric disorders including both BD and SZ [22,23].
rs1344706 in ZNF804A and schizophrenia (P = 1.61 ×
10-7), and found strong evidence when the affected
phenotype included patients with bipolar disorder
(P = 9.96 × 10-9) . Several replication studies
confirmed the association [24-27]. Meta–analysis of a
larger dataset found very strong evidence for association
between rs1344706 and schizophrenia (P = 2.54 × 10-11)
anda combined schizophrenia/bipolar
(P = 4.1 × 10-13) . Balog et al.,  investigated the
relationship between rs1344706 in ZNF804A and atten-
tion in 200 healthy volunteers and found a significant
association with a measure of the executive control
attention network. One recent study examined six SNPs
in five genes in adult ADHD, and concluded that the six
SNPs including rs1344706 in ZNF804A, which showed
strong evidence of association with bipolar disorder, did
not appear to be associated with ADHD .
As ADHD and BD are both highly heritable, show
comorbidity with each other and an increased cross-
disorder familial risk [30,31], the aim of the present
study was to provide further investigation of genetic
evidence linking ADHD and bipolar disorder. We
examine the role of the rs1344706 polymorphism in
ZNF804A in two clinical ADHD samples from the
UK and Taiwan.
Materials and methods
The UK ADHD sample
DNA was collected from 180 ADHD combined subtype
probands. Both parents were available for 116 families,
and only the mother was available for 64 families.
Ninety-six percent of the sample was male. Cases were
recruited from child behaviour clinics and referred for
assessment if they were thought by experienced clini-
cians to have a diagnosis of combined subtype ADHD
under DSM-IV criteria, with no significant Axis I co-
morbidity apart from oppositional defiant disorder
(ODD, 5.5% of sample) and conduct disorder (CD, 15.5%
of sample). Intelligence quotient (IQ) was assessed using
the Wechsler Intelligence Scale for Children-Third
Edition (WISC-III). Exclusion criteria included IQ less
than 70, neurological disorders, brain damage or autism.
Only those individuals fulfilling the recruitment criteria
after completion of research assessments were included
in the study. All probands were of European-Caucasian
origin. The age range was 5–15 years at the time of
assessment (mean 10.41, SD 2.34). Parents were inter-
viewed with a modified version of the Child and Adoles-
cent Psychiatric Assessment (CAPA) . Information
on ADHD symptoms at school was obtained using the
teacher Conner’s revised questionnaire . The sub-
jects gave their written informed consent and were
approved by the ethical committee of King’s College
London (Reference number: G9814668).
Taiwanese ADHD sample
ADHD diagnosed between the ages of 5–15 years
(mean 8.96, SD 2.60), from both parents for 114 fa-
milies of the ADHD probands and from only the
mother for 59 families or only the father for 39 fa-
milies. ADHD cases were ascertained from Child
Psychiatric Clinics in the Chang Gung Memorial Hos-
pital in Taipei area, Taiwan. The diagnosis of ADHD
was made under DSM-IV criteria following comple-
tion of a standard maternal interview  and com-
pletion of Conners’ parent and teacher revised rating
scales . Seventy-eight percent of the sample had
combined subtype ADHD and 22% had inattentive
subtype ADHD, with no co-morbid disorders apart
from ODD (5.2%), CD (9.4%) and Tourettes syndrome
(1.8%). Cases with autism were excluded from the
study. Eighty-nine percent of the sample was male,
87% had IQ greater than 69 and 13% had IQ between
consent, and were approved by the Institutional Re-
view Board, Chang Gung Memorial Hospital, Taiwan
(Reference number: 96-0058B).
Xu et al. BMC Research Notes 2013, 6:29
Page 2 of 5
The rs1344706 polymorphism was genotyped using a
TaqManWSNP genotyping assay (Assay ID: C_2834835_10)
on a 7900HT sequence detection system (Applied Biosys-
tems). The distribution of the genotypes did not deviate
from Hardy-Weinberg equilibrium (P >0.05).
Genotype data from probands and parents were analysed
using the transmission disequilibrium test (TDT) imple-
mented in the UNPHASED program (TDTPHASE) .
Population frequencies for SNP rs1344706 (an A/C poly-
morphism) were estimated from parental genotypes. For
the UK and the Taiwanese sample the A-allele frequency
was 61% and 55%, respectively. There was no significant
difference in allele frequencies between the two popula-
frequencies did not deviate from Hardy–Weinberg equi-
librium in either population.
TDT analysis (Table 1) showed no evidence of
increased transmission of the A allele in either of the
samples (Taiwan: χ2= 0.012, P = 0.91; UK: χ2= 0.667,
P = 0.41). When the two datasets were combined, the A
allele was still not significantly over-transmitted to
affected probands (χ2= 0.458, P = 0.50).
We further explored the subtypes of ADHD. We
found that there was no association between rs1344706
and ADHD in the subgroup of the Taiwanese sample
with the inattentive subtype (χ2=0.604, P = 0.437). We
were not able to investigate the hyperactive-impulsive
subtype separately because neither samples included
any such cases. To investigate whether there were any
associations with the specific symptom domains of
ADHD, we therefore completed an additional analysis
using quantitative ratings of parent rated inattentive
and hyperactive-impulsive symptoms using quantitative
UNPHASED program. The results from QPDT analysis
showed that the A allele of rs1344706 was not asso-
ciated with either symptom domain in samples from UK
(Ζ-score = −0.214; P = 0.830 for inattentive symptoms;
Ζ-score = 0.416;
symptoms) or Taiwan (Ζ-score = 0.253; P = 0.801 for in-
Ζ-score = 0.220;
hyperactive-impulsive symptoms). When the two data-
sets were combined, the A allele was still not significantly
associated with either symptom domain (Ζ-score=
−0.293; P=0.769 for inattentive symptoms; Ζ-score=
0.049; P=0.961 for hyperactive-impulsive symptoms).
P = 0.677 forhyperactive-impulsive
P = 0.826 for
In this study we set out to investigate association be-
tween SNP rs1344706 in the ZNF804A gene, which was
previously found to be associated with BD, and ADHD
in two independent ADHD samples from the UK and
Taiwan. No association was observed between this poly-
morphism and ADHD in either sample or when the two
samples were pooled together. We further investigated
the association on specific symptom subgroups of
ADHD. We found no association with the subgroup of
the Taiwanese samples with DSM-IV inattentive subtype.
Furthermore, using a quantitative trait approach there
was no evidence of association with quantitative ratings
of either inattentive or hyperactive-impulsive symptoms
in either sample.
The human ZNF804A gene is located on the long arm
of chromosome 2 at the 2q32.1 and ZNF804A encodes
the transcription factor zinc-finger protein 804A. SNP
rs1344706 lies in intron 2 of ZNF804A and the A allele
is predicted to enhance the maintenance of binding sites
for brain-expressed transcription factors . ZNF804A
gene shows strong evidence of association with both BD
and SZ from GWAS [22,23]. The association between
SNPs in the Zinc finger gene and ADHD has been sug-
gested before, but a study investigating the relationship
between six SNPs reported to be associated with BD,
including SNP rs1344706, were not associated in a sam-
ples of adults with ADHD. However, a weak association
was however observed in the study between rs1344706
and a positive MDQ score, suggesting a possible asso-
ciation with risk for the development of mood symptoms
in adult patients with ADHD . Data from another
study suggest that rs1344706 is associated with increased
response latency on a task assessing the executive control
network of attention in healthy adult volunteers .
Table 1 Results of TDT analysis for rs1344706 polymorphism
UK samplesTaiwanese samplesCombined samples
Transmitted 44 5240 41 84 93
χ2, df (P-value)
52 4441 409384
0.667, 1df (0.41) 0.012, 1df (0.91)0.458, 1df (0.50)
Xu et al. BMC Research Notes 2013, 6:29
Page 3 of 5
In our study we used family-based ADHD data from
the UK and Taiwan to investigate the role between
rs1344706 and ADHD. The study presents several li-
mitations that need to be considered. The sample was
relatively small and might therefore be underpowered to
exclude very small genetic effects. Furthermore, the sub-
group with inattentive subtype ADHD was only 22% of
the Taiwanese sample and none of the UK sample. Only
one polymorphism was genotyped in this gene, therefore
we cannot exclude the possibility of association between
multiple SNP haplotypes and ADHD.
This study found no evidence of an association between
SNP rs1344706 in ZNF804A and ADHD in UK and
Taiwanese samples. Due to the limitation of sample size
in our study and the fact that, to our knowledge, there is
only one published study examining association between
rs1344706 and ADHD in adult samples, further associ-
ation studies are required to investigate the role of the
high-risk ZNF804A SNPs in ADHD. ZNF804A is a pro-
tein currently of unknown function. However, the risk
allele of rs1344706 associated with other major mental
illnesses has been shown to be associated with higher
ZNF804A expression . Further work should focus on
identifying any additional functional polymorphisms of
this gene for investigation in further samples of clinical
disorders that share genetic risks with either bipolar dis-
order or schizophrenia.
The authors declare that they have no competing interests.
XX selected the SNP, performed genotyping and drafted the manuscript. GB
supervised the study and revised the manuscript. LL and BS analysed genetic
data. UMP helped to do genotyping. CKC, YSH and YYW provided the
Taiwanese DNA samples and clinical data. CKC also revised the manuscript.
PA supervised the study and revised the paper. All authors contributed to
the final critical revision of the manuscript.
This research was funded by The Wellcome Trust (No.079314/4/2/06/2). The
study was also supported by the Department of Psychiatry of Chang Gung
Memorial Hospital in Taiwan. We thank Dr Karim Malki who helped revise
the manuscript and anonymous reviewers for their helpful suggestions. We
also thank the families who took part in this research and Dr Keeley Brookes
who helped prepare the UK samples.
1MRC Social, Genetic and Developmental Psychiatry Centre, Institute of
Psychiatry, King’s College London, London, UK.2School of Medicine, King’s
College London, London, UK.3Department of Psychiatry, Chang Gung
Memorial Hospital, Taoyuan, Taiwan.4Chang Gung University School of
Medicine, Taoyuan, Taiwan.5Division of Mental Health & Drug Abuse
Research, National Health Research Institutes, Taoyuan, Taiwan.
Received: 10 July 2012 Accepted: 23 January 2013
Published: 26 January 2013
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Cite this article as: Xu et al.: Investigation of the ZNF804A gene
polymorphism with genetic risk for bipolar disorder in attention deficit
hyperactivity disorder. BMC Research Notes 2013 6:29.
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