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

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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