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
Western University Health Sciences, Graduate School of Biomedical Sciences, Pomona, CA.
Eotvos Loránd University, Institute of Psychology, Budapest, Hungary.
Curr Psychopharmacol. 2021 Feb 15;10. doi: 10.2174/2211556010666210215155509.
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.
The primary issue involves the question of whether there exists a mixed hypo or hyper-dopaminergia in this population.
Genetic Addiction Risk Score (GARS®) testing was carried out of 24 Caucasians of ages 12-19, derived from families with RDS.
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%).
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.
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。
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。
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。
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%)。
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。