Potential Role of <i>ADRA2A</i> Genetic Variants in the Etiology of ADHD Comorbid With Tic Disorders

Xu, Defeng; Liu, Lu; Li, Haimei; Sun, Li; Yang, Li; Qian, Qiujin; Wang, Yufeng

doi:10.1177/1087054718757646

Cited by 3 publications

(1 citation statement)

References 47 publications

(59 reference statements)

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“…Hence, noradrenergic genes might reflect neurobiological commonalities and thus elucidate the neurobiological background of TD + ADHD. Xu et al [ 39 ] investigated the potential role of adrenergic ADRA2A genetic variants. Two single nucleotide polymorphisms (SNPs) of ADRA2A were genotyped and analyzed in 936 normal controls and 1815 ADHD probands, including 1249 trios.…”

Section: Level “Genetical and Environmental Risk Factors”mentioning

confidence: 99%

Co-Occurrence of Tic Disorders and Attention-Deficit/Hyperactivity Disorder—Does It Reflect a Common Neurobiological Background?

Rothenberger

Heinrich

2022

Biomedicines

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Background: The co-existence of tic disorders and attention-deficit/hyperactivity disorder (TD + ADHD) has proven to be highly important in daily clinical practice. The factor ADHD is not only associated with further comorbidities, but also has a long-term negative psychosocial effect, while the factor TD is usually less disturbing for the major part of the patients. It remains unclear how far this is related to a different neurobiological background of the associated disorders or whether TD + ADHD reflects a common one. Objective: This review provides an update on the neurobiological background of TD + ADHD in order to better understand and treat this clinical problem, while clarifying whether an additive model of TD + ADHD holds true and should be used as a basis for further clinical recommendations. Method: A comprehensive research of the literature was conducted and analyzed, including existing clinical guidelines for both TD and ADHD. Besides genetical and environmental risk factors, brain structure and functions, neurophysiological processes and neurotransmitter systems were reviewed. Results: Only a limited number of empirical studies on the neurobiological background of TD and ADHD have taken the peculiarity of co-existing TD + ADHD into consideration, and even less studies have used a 2 × 2 factorial design in order to disentangle the impact/effects of the factors of TD versus those of ADHD. Nevertheless, the assumption that TD + ADHD can best be seen as an additive model at all levels of investigation was strengthened, although some overlap of more general, disorder non-specific aspects seem to exist. Conclusion: Beyond stress-related transdiagnostic aspects, separate specific disturbances in certain neuronal circuits may lead to disorder-related symptoms inducing TD + ADHD in an additive way. Hence, within a classificatory categorical framework, the dimensional aspects of multilevel diagnostic-profiling seem to be a helpful precondition for personalized decisions on counselling and disorder-specific treatment in TD + ADHD.

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Section: Level “Genetical and Environmental Risk Factors”mentioning

confidence: 99%

Co-Occurrence of Tic Disorders and Attention-Deficit/Hyperactivity Disorder—Does It Reflect a Common Neurobiological Background?

Rothenberger

Heinrich

2022

Biomedicines

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Influence of Receptor Polymorphisms on the Response to α-Adrenergic Receptor Blockers in Pheochromocytoma Patients

et al. 2022

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Background: Presurgical treatment with an α-adrenergic receptor blocker is recommended to antagonize the catecholamine-induced α-adrenergic receptor mediated vasoconstriction in patients with pheochromocytoma or sympathetic paraganglioma (PPGL). There is, however, a considerable interindividual variation in the dose-response relationship regarding the magnitude of blood pressure reduction or the occurrence of side effects. We hypothesized that genetically determined differences in α-adrenergic receptor activity contribute to this variability in dose-response relationship. Methods: Thirty-one single-nucleotide polymorphisms (SNPs) of the α1A, α1B, α1D adrenoreceptor (ADRA1A, ADRA1B, ADRA1D) and α2A, α2B adrenoreceptor (ADRA2A, ADRA2B) genes were genotyped in a group of 116 participants of the PRESCRIPT study. Haplotypes were constructed after determining linkage disequilibrium blocks. Results: The ADRA1B SNP rs10515807 and the ADRA2A SNPs rs553668/rs521674 were associated with higher dosages of α-adrenergic receptor blocker (p < 0.05) and with a higher occurrence of side effects (rs10515807) (p = 0.005). Similar associations were found for haplotype block 6, which is predominantly defined by rs10515807. Conclusions: This study suggests that genetic variability of α-adrenergic receptor genes might be associated with the clinically observed variation in beneficial and adverse therapeutic drug responses to α-adrenergic receptor blockers. Further studies in larger cohorts are needed to confirm our observations.

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Asthma and Post-Asthmatic Fibrosis: A Search for New Promising Molecular Markers of Transition from Acute Inflammation to Pulmonary Fibrosis

et al. 2022

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Asthma is a heterogeneous pulmonary disorder, the progression and chronization of which leads to airway remodeling and fibrogenesis. To understand the molecular mechanisms of pulmonary fibrosis development, key genes forming the asthma-specific regulome and involved in lung fibrosis formation were revealed using a comprehensive bioinformatics analysis. The bioinformatics data were validated using a murine model of ovalbumin (OVA)-induced asthma and post-asthmatic fibrosis. The performed analysis revealed a range of well-known pro-fibrotic markers (Cat, Ccl2, Ccl4, Ccr2, Col1a1, Cxcl12, Igf1, Muc5ac/Muc5b, Spp1, Timp1) and a set of novel genes (C3, C3ar1, Col4a1, Col4a2, Cyp2e1, Fn1, Thbs1, Tyrobp) mediating fibrotic changes in lungs already at the stage of acute/subacute asthma-driven inflammation. The validation of genes related to non-allergic bleomycin-induced pulmonary fibrosis on asthmatic/fibrotic lungs allowed us to identify new universal genes (Col4a1 and Col4a2) associated with the development of lung fibrosis regardless of its etiology. The similarities revealed in the expression profiles of nodal fibrotic genes between asthma-driven fibrosis in mice and nascent idiopathic pulmonary fibrosis in humans suggest a tight association of identified genes with the early stages of airway remodeling and can be considered as promising predictors and early markers of pulmonary fibrosis.

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Potential Role of ADRA2A Genetic Variants in the Etiology of ADHD Comorbid With Tic Disorders

Abstract: ADRA2A may be associated with ADHD+TD, especially in males.

Cited by 3 publications

References 47 publications

Co-Occurrence of Tic Disorders and Attention-Deficit/Hyperactivity Disorder—Does It Reflect a Common Neurobiological Background?

Co-Occurrence of Tic Disorders and Attention-Deficit/Hyperactivity Disorder—Does It Reflect a Common Neurobiological Background?

Influence of Receptor Polymorphisms on the Response to α-Adrenergic Receptor Blockers in Pheochromocytoma Patients

Asthma and Post-Asthmatic Fibrosis: A Search for New Promising Molecular Markers of Transition from Acute Inflammation to Pulmonary Fibrosis

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