ASSOCIATIONS BETWEEN VARIATIONS IN TPH1, TPH2
AND SLC6A4 GENES AND POSTPARTUM DEPRESSION:
A STUDY IN THE JORDANIAN POPULATION Khabour OF1, Amarneh BH2, Bani Hani EA3, Lataifeh IM4 *Corresponding Author: Dr. Omar F. Khabour, Associate Professor of Molecular Genetics, Department of Medical
Laboratory, Sciences, Jordan University of Science and Technology, PO Box 3030, Irbid 22110, Jordan; Tel.:
+962-2-720-1000 ext. 23784; Fax: +962-2-720-1087; E-mail: khabour@just.edu.jo page: 41
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INTRODUCTION
Postpartum depression (PPD) occurs in 20.0-
50.0% of women who have recently given birth, and
may extend during the first year after delivery [1,2]. The
symptoms of PPD include feeling of being alone, sleep
deprivation, decreased desire for food, regular occurrence
of unstable, disproportional emotional displays,
and to a lesser extent, recurrent thoughts of harming
oneself and/or the child [1,2]. Depression is a complex
disorder, such that environmental as well as genetic
factors, may play a role in developing the disease.
The neurotransmitter serotonin plays a role in
sleep, appetite, emotions, body temperature and
blood pressure [3]. Disruption of serotonergic neurotransmission
is implicated in the development of
many psychiatric diseases such as depression and
bipolar disorder [4]. Therefore, variations in genes involved
in biosynthesis, transmission and metabolism
of serotonin are candidates for predisposing to PPD.
Among such candidates are tryptophan hydroxylase-1
(TPH1) (218A>C), and tryptophan hydroxylase-2 (TPH2) (1463G>A) genes that code for tryptophan
hydroxylase, the rate limiting enzyme in the conversion
of tryptophan into serotonin [5]. The TPH1
gene is located on chromosome 11, spans 29 kb, and
has 11 exons [6]. The gene is expressed mainly in
the pineal gland as well as in the peripheral tissues
[7]. Among the polymorphisms of the TPH1 gene is
the 218A>C (rs1800532) variation in intron 7 that
has been shown to affect the expression of the gene
[8,9]. Variations in TPH1 including 218A>C polymorphism,
have been shown to be associated with
bipolar disorder, suicidal behavior, alcoholism, and
aggression-related traits [10,11]. The TPH2 gene is
located on chromosome 12 and spans 93.5 kb with
11 exons. It is predominantly expressed in the brainstem
[7]. Zhang et al. [12] identified a functional a
polymorphism (1463G>A) in the TPH2 gene that
results in substitution of a highly conserved arginine
by a histidine (Arg441His) and the subsequent alterations
in enzyme activity [12]. Genetic variations in
TPH2 have been shown to be associated with suicide,
attention-deficit and hyperactivity disorder, autism
and depression [13,14]. Another candidate is serotonin
transporter gene solute carrier, serotonin carrier
family 6, member 4 (SLC6A4) which encodes the
human serotonin transporter that plays an important
role in terminating the synaptic action of serotonin
and recycles it into the presynaptic neurotransmitter
pool [15]. A long (L) and a short (S) variant in
the transcriptional control region upstream of the
SLC6A4 coding sequence was reported [16]. In vitro
analysis showed that the basal activity of the L form
was about three-fold higher than that of the S variant
[16]. This variant has been shown to be associated
with neuroticism [17] and depression [18-20].
In this study, we investigated the association
between TPH1, TPH2 and the SLC6A4 (L/S variant)
with PPD in the Jordanian population. In addition,
we examined the possible correlation between
socio-demographic, intra-partum and psychosocial
variables with PPD.
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