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Autism Spectrum Disorders and Drug Addiction: Common Pathways Common Molecules Distinct Disorders?

机译:自闭症谱系障碍和药物成瘾:常见途径常见分子不同疾病?

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摘要

Autism spectrum disorders (ASDs) and drug addiction do not share substantial comorbidity or obvious similarities in etiology or symptomatology. It is thus surprising that a number of recent studies implicate overlapping neural circuits and molecular signaling pathways in both disorders. The purpose of this review is to highlight this emerging intersection and consider implications for understanding the pathophysiology of these seemingly distinct disorders. One area of overlap involves neural circuits and neuromodulatory systems in the striatum and basal ganglia, which play an established role in addiction and reward but are increasingly implicated in clinical and preclinical studies of ASDs. A second area of overlap relates to molecules like Fragile X mental retardation protein (FMRP) and methyl CpG-binding protein-2 (MECP2), which are best known for their contribution to the pathogenesis of syndromic ASDs, but have recently been shown to regulate behavioral and neurobiological responses to addictive drug exposure. These shared pathways and molecules point to common dimensions of behavioral dysfunction, including the repetition of behavioral patterns and aberrant reward processing. The synthesis of knowledge gained through parallel investigations of ASDs and addiction may inspire the design of new therapeutic interventions to correct common elements of striatal dysfunction.
机译:自闭症谱系障碍(ASD)和药物成瘾在病因学或症状学上没有明显的合并症或明显相似之处。因此,令人惊讶的是,许多最新研究都暗示了这两种疾病中重叠的神经回路和分子信号传导途径。这篇综述的目的是强调这一新兴的交叉点,并考虑对理解这些看似独特的疾病的病理生理学意义。重叠的一个领域涉及纹状体和基底神经节中的神经回路和神经调节系统,它们在成瘾和奖赏中起着确定的作用,但越来越多地涉及ASD的临床和临床前研究。重叠的第二个领域涉及诸如脆性X智力低下蛋白(FMRP)和甲基CpG结合蛋白2(MECP2)之类的分子,这些分子以其对症状性ASD的发病机理的贡献而闻名,但最近被证明可以调节对成瘾性药物暴露的行为和神经生物学反应。这些共享的途径和分子指向行为功能障碍的共同维度,包括行为模式的重复和异常奖励过程。通过对ASD和成瘾的平行研究获得的知识的综合可能会启发设计新的治疗性干预措施,以纠正纹状体功能障碍的常见要素。

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