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In Search of Reward Deficiency Syndrome (RDS)-free Controls: The "Holy Grail" in Genetic Addiction Risk Testing.寻找无奖赏缺乏综合征(RDS)的对照:基因成瘾风险测试中的“圣杯”。
Curr Psychopharmacol. 2020;9(1):7-21.
2
Neuropharmacological and Neurogenetic Correlates of Opioid Use Disorder (OUD) As a Function of Ethnicity: Relevance to Precision Addiction Medicine.神经药理学和神经遗传学与阿片类药物使用障碍(OUD)的相关性,以及其与种族的关系:对精准成瘾医学的意义。
Curr Neuropharmacol. 2020;18(7):578-595. doi: 10.2174/1570159X17666191118125702.
3
Neonatal Nicotine Exposure Primes Midbrain Neurons to a Dopaminergic Phenotype and Increases Adult Drug Consumption.新生儿尼古丁暴露使中脑神经元呈现多巴胺能表型,并增加成年期药物消耗。
Biol Psychiatry. 2019 Sep 1;86(5):344-355. doi: 10.1016/j.biopsych.2019.04.019. Epub 2019 Apr 24.
4
Opioid Substitution Therapy: Achieving Harm Reduction While Searching for a Prophylactic Solution.阿片类药物替代疗法:在寻求预防性解决方案的同时实现减少伤害
Curr Pharm Biotechnol. 2019;20(3):180-182. doi: 10.2174/138920102003190422150527.
5
Pro-Dopamine Regulator (KB220) A Fifty Year Sojourn to Combat Reward Deficiency Syndrome (RDS): Evidence Based Bibliography (Annotated).促多巴胺调节剂(KB220):对抗奖赏缺乏综合征(RDS)的五十年征程:循证文献目录(注释版)
CPQ Neurol Psychol. 2018;1(2). Epub 2018 Dec 4.
6
Dysregulation of Dopaminergic Regulatory Factors TH, Nurr1, and Pitx3 in the Ventral Tegmental Area Associated with Neuronal Injury Induced by Chronic Morphine Dependence.多巴胺调节因子 TH、Nurr1 和 Pitx3 在腹侧被盖区的失调与慢性吗啡依赖诱导的神经元损伤有关。
Int J Mol Sci. 2019 Jan 10;20(2):250. doi: 10.3390/ijms20020250.
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Introducing Precision Addiction Management of Reward Deficiency Syndrome, the Construct That Underpins All Addictive Behaviors.介绍奖赏缺乏综合征的精准成瘾管理,这一构成所有成瘾行为基础的概念。
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Analysis of Evidence for the Combination of Pro-dopamine Regulator (KB220PAM) and Naltrexone to Prevent Opioid Use Disorder Relapse.促多巴胺调节剂(KB220PAM)与纳曲酮联合预防阿片类物质使用障碍复发的证据分析
EC Psychol Psychiatr. 2018 Aug;7(8):564-579. Epub 2018 Jul 30.
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Promoting Precision Addiction Management (PAM) to Combat the Global Opioid Crisis.推动精准成瘾管理(PAM)以应对全球阿片类药物危机。
Biomed J Sci Tech Res. 2018 Jan 7;2(2):1-4. doi: 10.26717/BJSTR.2018.02.000738.
10
The Catechol-O-Methyltransferase and Dopamine Transporter Genes Moderated the Impact of Peer Relationships on Adolescent Depressive Symptoms: A Gene-Gene-Environment Study.儿茶酚-O-甲基转移酶和多巴胺转运体基因调节同伴关系对青少年抑郁症状的影响:一项基因-基因-环境研究。
J Youth Adolesc. 2018 Nov;47(11):2468-2480. doi: 10.1007/s10964-018-0925-3. Epub 2018 Sep 21.

青少年大脑发育过程中表观遗传状态高多巴胺能(过剩)和遗传性状低多巴胺能(不足)的探索。

Exploration of Epigenetic State Hyperdopaminergia (Surfeit) and Genetic Trait Hypodopaminergia (Deficit) During Adolescent Brain Development.

作者信息

Blum Kenneth, Bowirrat Abdalla, Gondre Lewis Marjorie C, Simpatico Thomas A, Ceccanti Mauro, Steinberg Bruce, Modestino Edward J, Thanos Panayotis K, Baron David, McLaughlin Thomas, Brewer Raymond, Badgaiyan Rajendra D, Ponce Jessica Valdez, Lott Lisa, Gold Mark S

机构信息

Western University Health Sciences, Graduate School of Biomedical Sciences, Pomona, CA.

Eotvos Loránd University, Institute of Psychology, Budapest, Hungary.

出版信息

Curr Psychopharmacol. 2021 Feb 15;10. doi: 10.2174/2211556010666210215155509.

DOI:10.2174/2211556010666210215155509
PMID:34707969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8547282/
Abstract

BACKGROUND

The risk for all addictive drug and non-drug behaviors, especially, in the unmyelinated Prefrontal Cortex (PFC) of adolescents, is important and complex. Many animal and human studies show the epigenetic impact on the developing brain in adolescents, compared to adults. Some reveal an underlying hyperdopaminergia that seems to set our youth up for risky behaviors by inducing high quanta pre-synaptic dopamine release at reward site neurons. In addition, altered reward gene expression in adolescents caused epigenetically by social defeat, like bullying, can continue into adulthood. In contrast, there is also evidence that epigenetic events can elicit adolescent hypodopaminergia. This complexity suggests that neuroscience cannot make a definitive claim that all adolescents carry a hyperdopaminergia trait.

OBJECTIVE

The primary issue involves the question of whether there exists a mixed hypo or hyper-dopaminergia in this population.

METHOD

Genetic Addiction Risk Score (GARS®) testing was carried out of 24 Caucasians of ages 12-19, derived from families with RDS.

RESULTS

We have found that adolescents from this cohort, derived from RDS parents, displayed a high risk for any addictive behavior (a hypodopaminergia), especially, drug-seeking (95%) and alcohol-seeking (64%).

CONCLUSION

The adolescents in our study, although more work is required, show a hypodopaminergic trait, derived from a family with Reward Deficiency Syndrome (RDS). Certainly, in future studies, we will analyze GARS in non-RDS Caucasians between the ages of 12-19. The suggestion is first to identify risk alleles with the GARS test and, then, use well-researched precision, pro-dopamine neutraceutical regulation. This "two-hit" approach might prevent tragic fatalities among adolescents, in the face of the American opioid/psychostimulant epidemic.

摘要

背景

所有成瘾性药物和非药物行为的风险,尤其是在青少年未成熟的前额叶皮质(PFC)中,既重要又复杂。与成年人相比,许多动物和人体研究表明表观遗传学对青少年发育中的大脑有影响。一些研究揭示了一种潜在的多巴胺能亢进,它似乎通过在奖赏部位神经元诱导高量子的突触前多巴胺释放,使我们的年轻人倾向于冒险行为。此外,社会挫败(如欺凌)在表观遗传上导致的青少年奖赏基因表达改变可持续到成年期。相比之下,也有证据表明表观遗传事件可引发青少年多巴胺能减退。这种复杂性表明,神经科学不能确定地宣称所有青少年都具有多巴胺能亢进特征。

目的

主要问题涉及该人群中是否存在多巴胺能减退或亢进的混合状态。

方法

对来自患有奖赏缺乏综合征(RDS)家庭的24名12至19岁的白种人进行了遗传成瘾风险评分(GARS®)测试。

结果

我们发现,来自患有RDS父母家庭的这一队列中的青少年,对任何成瘾行为(多巴胺能减退)都表现出高风险,尤其是寻求毒品(95%)和寻求酒精(64%)。

结论

我们研究中的青少年,尽管还需要更多研究,但显示出一种多巴胺能减退特征,源自一个患有奖赏缺乏综合征(RDS)的家庭。当然,在未来的研究中,我们将分析12至19岁非RDS白种人的GARS。建议首先通过GARS测试识别风险等位基因,然后使用经过充分研究的精准促多巴胺神经营养调节方法。面对美国的阿片类药物/精神兴奋剂流行,这种“双管齐下”的方法可能预防青少年中的悲惨死亡。