治疗暴食症新药的前景:来自精神病理学和神经药理学的见解。

David J Heal, Sharon L Smith
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引用次数: 8

摘要

背景:暴食症(BED)是一种常见的精神疾病,具有不良的心理和代谢后果。利地安非他明(LDX)是唯一被批准的BED药物治疗。迫切需要治疗BED的新药。方法:对已发表的精神病理、药理和临床研究结果进行综合综述。结果:证据支持BED是一种与ADHD相似的冲动控制障碍的假设,包括对儿茶酚胺能药物的反应,例如LDX和dasotraline。理想的BED药物的目标产品特征(TPP)结合了治疗该疾病的精神病理驱动因素和独立的减肥效果。已证实对BED有效的药物具有共同的药理学;它们增强中枢去肾上腺素能和多巴胺能神经传递。由于注意缺陷多动障碍(ADHD)和BED的药物治疗之间的重叠,来自不同药理学类别的候选药物,已经在ADHD中失败,如果在BED中测试,预计也会失败。具有不同药理机制的药物在BED试验中的失败表明,许多可能的药物发现途径可能会被忽视。结论:(1)药物治疗BED的疗效取决于降低其核心精神病理的冲动性、强迫性和持久性,以及增强对饮食的认知控制。(2)分析表明,大量的药理机制不太可能在寻找有效的新型BED药物中产生效果。(3) BED最有希望的新治疗领域是那些增强去甲肾上腺素能和多巴胺能神经传递和/或那些对多动症有效的药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Prospects for new drugs to treat binge-eating disorder: Insights from psychopathology and neuropharmacology.

Prospects for new drugs to treat binge-eating disorder: Insights from psychopathology and neuropharmacology.

Prospects for new drugs to treat binge-eating disorder: Insights from psychopathology and neuropharmacology.

Prospects for new drugs to treat binge-eating disorder: Insights from psychopathology and neuropharmacology.

Background: Binge-eating disorder (BED) is a common psychiatric condition with adverse psychological and metabolic consequences. Lisdexamfetamine (LDX) is the only approved BED drug treatment. New drugs to treat BED are urgently needed.

Methods: A comprehensive review of published psychopathological, pharmacological and clinical findings.

Results: The evidence supports the hypothesis that BED is an impulse control disorder with similarities to ADHD, including responsiveness to catecholaminergic drugs, for example LDX and dasotraline. The target product profile (TPP) of the ideal BED drug combines treating the psychopathological drivers of the disorder with an independent weight-loss effect. Drugs with proven efficacy in BED have a common pharmacology; they potentiate central noradrenergic and dopaminergic neurotransmission. Because of the overlap between pharmacotherapy in attention deficit hyperactivity disorder (ADHD) and BED, drug-candidates from diverse pharmacological classes, which have already failed in ADHD would also be predicted to fail if tested in BED. The failure in BED trials of drugs with diverse pharmacological mechanisms indicates many possible avenues for drug discovery can probably be discounted.

Conclusions: (1) The efficacy of drugs for BED is dependent on reducing its core psychopathologies of impulsivity, compulsivity and perseveration and by increasing cognitive control of eating. (2) The analysis revealed a large number of pharmacological mechanisms are unlikely to be productive in the search for effective new BED drugs. (3) The most promising areas for new treatments for BED are drugs, which augment noradrenergic and dopaminergic neurotransmission and/or those which are effective in ADHD.

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