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注意缺陷多动障碍与奖励缺失综合征。

Attention-deficit-hyperactivity disorder and reward deficiency syndrome.

机构信息

Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA.

出版信息

Neuropsychiatr Dis Treat. 2008 Oct;4(5):893-918. doi: 10.2147/ndt.s2627.

Abstract

Molecular genetic studies have identified several genes that may mediate susceptibility to attention deficit hyperactivity disorder (ADHD). A consensus of the literature suggests that when there is a dysfunction in the "brain reward cascade," especially in the dopamine system, causing a low or hypo-dopaminergic trait, the brain may require dopamine for individuals to avoid unpleasant feelings. This high-risk genetic trait leads to multiple drug-seeking behaviors, because the drugs activate release of dopamine, which can diminish abnormal cravings. Moreover, this genetic trait is due in part to a form of a gene (DRD(2) A1 allele) that prevents the expression of the normal laying down of dopamine receptors in brain reward sites. This gene, and others involved in neurophysiological processing of specific neurotransmitters, have been associated with deficient functions and predispose individuals to have a high risk for addictive, impulsive, and compulsive behavioral propensities. It has been proposed that genetic variants of dopaminergic genes and other "reward genes" are important common determinants of reward deficiency syndrome (RDS), which we hypothesize includes ADHD as a behavioral subtype. We further hypothesize that early diagnosis through genetic polymorphic identification in combination with DNA-based customized nutraceutical administration to young children may attenuate behavioral symptoms associated with ADHD. Moreover, it is concluded that dopamine and serotonin releasers might be useful therapeutic adjuncts for the treatment of other RDS behavioral subtypes, including addictions.

摘要

分子遗传学研究已经确定了几个可能介导注意缺陷多动障碍(ADHD)易感性的基因。文献的共识表明,当“大脑奖励级联”出现功能障碍时,特别是在多巴胺系统中,导致低或低多巴胺能特征时,大脑可能需要多巴胺来避免个体产生不愉快的感觉。这种高风险的遗传特征导致了多种觅药行为,因为这些药物会激活多巴胺的释放,从而减轻异常的渴望。此外,这种遗传特征部分归因于一种基因(DRD(2) A1 等位基因)的形式,它阻止了多巴胺受体在大脑奖励部位的正常沉积。这种基因,以及其他涉及特定神经递质的神经生理加工的基因,与功能缺陷有关,并使个体容易产生成瘾、冲动和强迫行为倾向的高风险。有人提出,多巴胺能基因和其他“奖励基因”的遗传变异是奖励缺乏综合征(RDS)的重要共同决定因素,我们假设 RDS 包括 ADHD 作为一种行为亚型。我们进一步假设,通过基因多态性识别与基于 DNA 的定制营养补充剂联合进行早期诊断,可能会减轻与 ADHD 相关的行为症状。此外,结论认为多巴胺和 5-羟色胺释放剂可能是治疗其他 RDS 行为亚型(包括成瘾)的有用治疗辅助手段。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e4c/2626918/b14b5574a419/ndt-4-893f1.jpg

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