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العنوان
Study of the Serotonergic Gene 5-HT1B as a Risk Factor for the Development of Attention Deficit Hyperactive Disorder (ADHD) \
المؤلف
Hassaballah, Dalia Muhammed Saied.
هيئة الاعداد
مشرف / داليا محمد سعيد حسب الله
مشرف / فريدة الباز محمد الباز
مشرف / سالي سليمان زهرة
مشرف / طارق مصطفى كمال
تاريخ النشر
2017.
عدد الصفحات
226 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
طب الأطفال ، الفترة المحيطة بالولادة وصحة الطفل
تاريخ الإجازة
1/1/2017
مكان الإجازة
جامعة عين شمس - كلية الطب - طب الأطفـال
الفهرس
Only 14 pages are availabe for public view

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from 226

Abstract

ADHD is a common neurodevelopmental disorder that affects mainly children below age of 12 years and symptoms might continue into adolescents (Ginsberg et al., 2014). Patients with ADHD might show persistent pattern of attention deficits, hyperactivity or impulsiveness that is not appropriate for the patient’s age leading to various degrees of functional impairment (Kooij et al., 2010; Polanczyk et al., 2014).
Although the precise etiology of ADHD is still controversial, complex interactions between multiple genetic and environmental risk factors have been suggested (ADHD Institute, 2015). Serotonin dysregulation has been related to impulsive behavior in children, and thus has been hypothesized to play a causal role in ADHD (Kranzler et al., 2002; Banaschewski et al., 2010)
Furthermore, Serotonin regulates dopaminergic neurotransmission in some areas of the brain via several 5-HT receptors including 5-HT1B. Polymorphisms in the serotonin transporter gene have been associated with differential response to ADHD treatment (“ADHD Aetiology - Genetics, neurobiology, environment _ ADHD Institute,” n.d.). Moreover, Candidate gene studies of ADHD have produced substantial evidence implicating several genes in the etiology of the disorder (“ADHD Aetiology- Genetics, neurobiology, environment _ ADHD Institute,” n.d.).
The objective of this study was to study the association between the serotonergic gene 5-HT1B and the development of ADHD in a sample of Egyptian children. In particular, we wanted to examine distribution imbalance in G861C allele of the 5HT1B gene.
We conducted a case-control study of 50 patients with ADHD from the Child Psychiatry Clinic - Ain Shams University Hospital, Cairo, Egypt. Fifty controls were selected not to have the disease and matched on age and sex. All the studied patients were subjected to physical examination, psychiatric evaluation, genetic study and further evaluation was done by Conners parent rating scale for detection of severity of ADHD and IQ assessment using the Arabic version of Wechsler intelligence scale for children (WISC).
We noticed a male predominance in ADHD cases where they represent 88% of cases with male to female ratio 7:1 with ages range from 6 to 16 years old with (mean age 9.28, SD ± 2.26). Regarding consanguinity, 28% of parents of cases were consanguineous as opposed to 10% of controls which is statistically significant (p-value <0.05). In addition, family history was of significant statistical value (18% in cases, 0% in controls) (p-value <0.05).
In the current study, there was a tendency of G allele to segregate in homozygosity (58%) than C allele (4%) with more prevalence of G allele among patients group (75%). Similarly, in the control group, there was a tendency of G allele to segregate in homozygosity (60%). The C allele appeared only in heterozygous state (20%) with more prevalence of G allele (80%). Therefore, we observed patients and controls showed similar distribution with respect of G allele and C allele (No significant statistical difference, p>0.05). There were 29(58%) of patients carrying GG, similarly 30 (60%) controls showed GG-genotype. However, 4 (8%) patients were detected carrying CC and none in the control group, but this didn’t reach statistical significance.
Based on these findings, we concluded there was no significant association between 5HT1B and ADHD in this sample of Egyptian children. Patients and controls showed similar distribution with respect to the G allele and C allele of G861C of the 5HT1B receptor gene.