2017
DOI: 10.1038/srep45595
|View full text |Cite
|
Sign up to set email alerts
|

Polymorphisms of STS gene and SULT2A1 gene and neurosteroid levels in Han Chinese boys with attention-deficit/hyperactivity disorder: an exploratory investigation

Abstract: This study examined the relationships among polymorphisms of the STS gene and SULT2A1 gene, dehydroepiandrosterone (DHEA) and its sulfated form (DHEA-S), and characteristics of attention-deficit/hyperactivity disorder (ADHD). We used cheek swabs to obtain the genomic DNA of 200 ADHD male probands (mean age: 8.7 years), 192 patients’ mothers and 157 patients’ fathers. Three SNPs in the STS gene (rs6639786, rs2270112, and rs17268988) and one SNP in the SULT2A1 gene (rs182420) were genotyped. Saliva samples were … Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

0
3
0

Year Published

2019
2019
2024
2024

Publication Types

Select...
5
1
1

Relationship

1
6

Authors

Journals

citations
Cited by 10 publications
(5 citation statements)
references
References 69 publications
0
3
0
Order By: Relevance
“…The exposure of STS only possesses in the specific areas of the brain, which are basal ganglia, frontal cortex, and thalamus (highly affected regions whose physiological function have a direct concern with ADHD) (Stergiakouli et al., 2011). The number of evidence ensures the role of STS in ADHD, cytogenetic deletions in males lead to encompassing the gene, which further leads to an increase in the susceptibility to disorder (Brookes et al., 2010; Wang et al., 2017). The DHEA(S) level has an inverse relationship with the symptomatology of ADHD, which can be enhanced by MPH treatment (Lee et al., 2008; Pallanti & Salerno, 2020).…”
Section: Animal Models Of Adhdmentioning
confidence: 99%
See 1 more Smart Citation
“…The exposure of STS only possesses in the specific areas of the brain, which are basal ganglia, frontal cortex, and thalamus (highly affected regions whose physiological function have a direct concern with ADHD) (Stergiakouli et al., 2011). The number of evidence ensures the role of STS in ADHD, cytogenetic deletions in males lead to encompassing the gene, which further leads to an increase in the susceptibility to disorder (Brookes et al., 2010; Wang et al., 2017). The DHEA(S) level has an inverse relationship with the symptomatology of ADHD, which can be enhanced by MPH treatment (Lee et al., 2008; Pallanti & Salerno, 2020).…”
Section: Animal Models Of Adhdmentioning
confidence: 99%
“…This model is based upon the number of findings that suggest the spontaneously hypertensive rat (SHR) model as an excellent hyperactive model to study ADHD (Leffa et al., 2018; Wang et al., 2017). According to the principle, the model is based on inbred strain derived from the Wistar‐Kyoto (WK) rat, there are several up‐regulatory as well as dawn‐regulatory pathological pathways that makes this model more reliable, For example, the impaired release of DA, due increase in D5 and D1 receptors density presynaptically, alteration in the fashion of release of noradrenergic system, down‐regulation of beta‐adrenoreceptors and various other aspects help to shape out this model and provide good face, predictive validities.…”
Section: Animal Models Of Adhdmentioning
confidence: 99%
“…Each factor index, as well as the FSIQ, has a population mean of 100 and a standard deviation of 15. The WISC-IV has been applied for Taiwanese school-aged children in several clinical studies [38,39].…”
Section: Neurocognitive Assessmentsmentioning
confidence: 99%
“…65,67 Deficiencies in the production of this enzymes are the etiology of diseases, can be fatal and incompatible with life, making them essential to the physiology. 68 69 Further, DHEA can be reduced to androstenediol by 17βhydroxysteroid dehydrogenase 1 (17β-HSD1; HSD17B1). 70 The isoenzymes 3β-hydroxysteroid dehydrogenase 1/2 (3β-HSD; HSD3B1 and HSD3B2, respectively) are responsible to convert DHEA into androstenedione and androstenediol into testosterone.…”
Section: Sex Steroid Hormones and Physiologymentioning
confidence: 99%
“…Androgen hormones biosynthesis. DHEA-S is converted in DHEA by the catalysis action of steroid sulfatase enzyme (STS; STS), while sulfotransferase 2A1 (ST2A1; SULT2A1) do the reverse way by conjugating sulfate to DHEA 69. Further, DHEA can be reduced to androstenediol by 17βhydroxysteroid dehydrogenase 1 (17β-HSD1; HSD17B1) 70.…”
mentioning
confidence: 99%