Pro-Dopamine Regulator - (KB220) to Balance Brain Reward Circuitry in Reward Deficiency Syndrome (RDS).

Journal of reward deficiency syndrome and addiction science Pub Date : 2017-01-01 Epub Date: 2017-04-28
Kenneth Blum, Marcelo Febo, Lyle Fried, David Baron, Eric R Braverman, Kristina Dushaj, Mona Li, Zsolt Demetrovics, Rajendra D Badgaiyan
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Abstract

We are faced with a worldwide opiate/opioid epidemic that is devastating. According to the Centers for Disease Control and Prevention (CDC), at least 127 people, young and old, are dying every day in America due to narcotic overdose. The Food and Drug Administration (FDA) has approved Medication-Assisted Treatments (MATs) for opiate/opioids as well as alcohol and nicotine. The mechanism of action of most MATS favors either blocking of dopaminergic function or a form of Opiate Substitution Therapy (OST). These treatment options are adequate for short-term treatment of the symptoms of addiction and harm reduction but fail long-term to deal with the cause or lead to recovery. There is a need to continue to seek better treatment options. This mini-review is the history of the development of one such treatment; a glutaminergic-dopaminergic optimization complex called KB220. Growing evidence indicates that brain reward circuitry controls drug addiction, in conjunction with "anti-reward systems" as the "anti-reward systems" can be affected by both glutaminergic and dopaminergic transmission. KB220 may likely alter the function of these regions and provide for the possible eventual balancing the brain reward system and the induction of "dopamine homeostasis." Many of these concepts have been reported elsewhere and have become an integral part of the addiction science literature. However, the concise review may encourage readership to reconsider these facts and stimulate further research focused on the impact that the induction of "dopamine homeostasis" may have on recovery and relapse prevention.

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亲多巴胺调节剂- (KB220)在奖励缺乏综合征(RDS)中平衡大脑奖励回路。
我们面临着全球性的阿片类药物流行病,这是毁灭性的。根据美国疾病控制与预防中心(CDC)的数据,在美国,每天至少有127人(无论老少)死于麻醉药物过量。美国食品和药物管理局(FDA)已经批准了阿片类药物/阿片类药物以及酒精和尼古丁的药物辅助治疗(MATs)。大多数MATS的作用机制倾向于阻断多巴胺能功能或一种形式的阿片替代疗法(OST)。这些治疗方案在短期内足以治疗成瘾症状和减少危害,但在长期内无法解决原因或导致康复。有必要继续寻求更好的治疗方案。这篇小型综述是一种此类治疗的发展历史;谷氨酰胺能-多巴胺能优化复合物KB220越来越多的证据表明,大脑奖励回路与“反奖励系统”一起控制药物成瘾,因为“反奖励系统”可以受到谷氨酰胺能和多巴胺能传递的影响。KB220可能会改变这些区域的功能,并提供可能的最终平衡大脑奖励系统和诱导“多巴胺稳态”。许多这些概念已经在其他地方被报道过,并且已经成为成瘾科学文献的一个组成部分。然而,这篇简明的综述可能会鼓励读者重新考虑这些事实,并激发进一步的研究,重点关注“多巴胺稳态”诱导对康复和复发预防的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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