Genetic variations influence brain changes in patients with attention-deficit hyperactivity disorder.
Genetic variations influence brain changes in patients with attention-deficit hyperactivity disorder.
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遗传变异会影响注意力缺陷多动障碍患者的大脑变化。
DOI：
10.1038/s41398-021-01473-w
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发表时间：
2021-06-05
影响因子：
6.8
通讯作者：
Haris M
中科院分区：
文献类型：
--
作者：
Yadav SK;Bhat AA;Hashem S;Nisar S;Kamal M;Syed N;Temanni MR;Gupta RK;Kamran S;Azeem MW;Srivastava AK;Bagga P;Chawla S;Reddy R;Frenneaux MP;Fakhro K;Haris M
注意力缺陷多动障碍 (ADHD) 是一种儿童期发病的神经和神经发育障碍，其特征是持续的注意力不集中、冲动、烦躁和多动。 55-66% 的病例可能会从儿童期一直持续到成年期。尽管 ADHD 的确切病因尚不完全清楚，但它被认为是一种多因素和异质性疾病，具有多种影响因素，例如遗传性、辅助神经发育问题、严重脑损伤、神经炎症、近亲结婚、早产和接触环境毒素。神经影像学和神经发育评估可能有助于探索遗传变异对 ADHD 神经心理生物学的可能作用。多项遗传学研究观察到，神经心理生物学功能的各个方面都存在很强的遗传关联，包括多动症的神经异常和神经发育迟缓。神经影像学和分子基因组学的进步提供了分析遗传变异及其失调途径对各种神经和精神疾病（包括多动症）的结构和功能衍生脑成像表型的影响的机会。最近，神经影像基因组研究观察到脑成像表型与 ADHD 遗传易感性之间存在显着关联。将神经影像衍生的表型与基因组学相结合，破译了各种神经生物学途径，可用于开发新型临床生物标志物、新的治疗方式以及 ADHD 患者的治疗干预措施。在这篇综述中，我们讨论了 ADHD 的神经生物学，特别强调 ADHD 大脑的结构和功能变化及其与利用成像遗传学方法的复杂基因组变异的相互作用。我们还强调了据称与多动症的发展有关的遗传变异，以及这些变异如何反过来影响大脑回路功能和相关行为。除了回顾影像遗传学研究之外，我们还研究了在不同生物复杂性水平上采取补充方法的必要性，并强调了结合和整合结果以探索 ADHD 疾病涉及的生物途径的重要性。这些方法包括动物模型、计算生物学、生物信息学分析和多模态成像遗传学研究。
Attention-deficit hyperactivity disorder (ADHD) is a neurological and neurodevelopmental childhood-onset disorder characterized by a persistent pattern of inattentiveness, impulsiveness, restlessness, and hyperactivity. These symptoms may continue in 55–66% of cases from childhood into adulthood. Even though the precise etiology of ADHD is not fully understood, it is considered as a multifactorial and heterogeneous disorder with several contributing factors such as heritability, auxiliary to neurodevelopmental issues, severe brain injuries, neuroinflammation, consanguineous marriages, premature birth, and exposure to environmental toxins. Neuroimaging and neurodevelopmental assessments may help to explore the possible role of genetic variations on ADHD neuropsychobiology. Multiple genetic studies have observed a strong genetic association with various aspects of neuropsychobiological functions, including neural abnormalities and delayed neurodevelopment in ADHD. The advancement in neuroimaging and molecular genomics offers the opportunity to analyze the impact of genetic variations alongside its dysregulated pathways on structural and functional derived brain imaging phenotypes in various neurological and psychiatric disorders, including ADHD. Recently, neuroimaging genomic studies observed a significant association of brain imaging phenotypes with genetic susceptibility in ADHD. Integrating the neuroimaging-derived phenotypes with genomics deciphers various neurobiological pathways that can be leveraged for the development of novel clinical biomarkers, new treatment modalities as well as therapeutic interventions for ADHD patients. In this review, we discuss the neurobiology of ADHD with particular emphasis on structural and functional changes in the ADHD brain and their interactions with complex genomic variations utilizing imaging genetics methodologies. We also highlight the genetic variants supposedly allied with the development of ADHD and how these, in turn, may affect the brain circuit function and related behaviors. In addition to reviewing imaging genetic studies, we also examine the need for complementary approaches at various levels of biological complexity and emphasize the importance of combining and integrating results to explore biological pathways involved in ADHD disorder. These approaches include animal models, computational biology, bioinformatics analyses, and multimodal imaging genetics studies.
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DOI：
10.1017/s1461145711001131
发表时间：
2012-02
期刊：
The international journal of neuropsychopharmacology
影响因子：
--
作者：
Buitelaar JK;Trott GE;Hofecker M;Waechter S;Berwaerts J;Dejonkheere J;Schäuble B
通讯作者：
Schäuble B
影响因子：
11.3
作者：
Brown AB;Biederman J;Valera E;Makris N;Doyle A;Whitfield-Gabrieli S;Mick E;Spencer T;Faraone S;Seidman L
通讯作者：
Seidman L
DOI：
10.1111/jcpp.12742
发表时间：
2017-08
期刊：
Journal of child psychology and psychiatry, and allied disciplines
影响因子：
--
作者：
van Ewijk H;Bralten J;van Duin EDA;Hakobjan M;Buitelaar JK;Heslenfeld DJ;Hoekstra PJ;Hartman C;Hoogman M;Oosterlaan J;Franke B
通讯作者：
Franke B
影响因子：
2
作者：
Acosta MT;Swanson J;Stehli A;Molina BS;MTA Team;Martinez AF;Arcos-Burgos M;Muenke M
通讯作者：
Muenke M
影响因子：
11
作者：
Arcos-Burgos, M.;Jain, M.;Muenke, M.
通讯作者：
Muenke, M.