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衰减性精神病综合征中衰减的失配负波预测精神病:加兰他敏-美金刚联合用药能否预防精神病?

Attenuated Mismatch Negativity in Attenuated Psychosis Syndrome Predicts Psychosis: Can Galantamine-Memantine Combination Prevent Psychosis?

作者信息

Koola Maju Mathew

机构信息

Department of Psychiatry and Behavioral Sciences, George Washington University School of Medicine and Health Sciences, Washington, District of Columbia, USA.

出版信息

Mol Neuropsychiatry. 2018 Oct;4(2):71-74. doi: 10.1159/000488797. Epub 2018 Jun 7.

Abstract

Although first proposed in 1987, early diagnosis and intervention of psychotic disorders has only recently become a priority in the field. The interest in clinical high risk (CHR) for psychosis skyrocketed after attenuated psychosis syndrome (APS) was added to the DSM-5. There is evidence that in individuals with APS, attenuated mismatch negativity (MMN: functioning of the auditory sensory memory system) is a robust biomarker that can predict transition to psychosis. The underlying pathophysiological mechanism of MMN is via the interaction of -methyl-D-aspartate (NMDA) and alpha-7 nicotinic acetylcholine (α-7nACh) receptors. Galantamine is an acetylcholinesterase inhibitor and a positive allosteric modulator of the α-7nACh receptors. Memantine is an NMDA receptor antagonist. Memantine has been shown to enhance MMN in people with schizophrenia. Although no studies with galantamine have measured MMN, encenicline, an α-7 nicotinic partial agonist, increased MMN in people with schizophrenia. MMN has been suggested as a potential biomarker with the galantamine-memantine combination for the treatment of neuropsychiatric disorders. Hence, the galantamine-memantine combination may enhance MMN, thereby preventing CHR to psychosis. With no treatments available, randomized controlled trials are warranted with the galantamine-memantine combination to delay or prevent conversion to psychosis in individuals with CHR.

摘要

尽管精神病性障碍的早期诊断和干预早在1987年就已被提出,但直到最近才成为该领域的一个优先事项。在《精神疾病诊断与统计手册》第五版(DSM-5)中加入了亚临床精神病综合征(APS)后,对精神病临床高危(CHR)的关注度急剧上升。有证据表明,在患有APS的个体中,亚临床失配负波(MMN:听觉感觉记忆系统的功能)是一种可靠的生物标志物,可以预测向精神病的转变。MMN的潜在病理生理机制是通过N-甲基-D-天冬氨酸(NMDA)和α-7烟碱型乙酰胆碱(α-7nACh)受体的相互作用。加兰他敏是一种乙酰胆碱酯酶抑制剂,也是α-7nACh受体的正变构调节剂。美金刚是一种NMDA受体拮抗剂。美金刚已被证明可增强精神分裂症患者的MMN。虽然尚无关于加兰他敏的研究测量过MMN,但一种α-7烟碱型部分激动剂恩西尼cline可增加精神分裂症患者的MMN。MMN已被认为是加兰他敏-美金刚联合治疗神经精神疾病的一种潜在生物标志物。因此,加兰他敏-美金刚联合用药可能增强MMN,从而预防CHR发展为精神病。由于目前尚无有效治疗方法,有必要对加兰他敏-美金刚联合用药进行随机对照试验,以延缓或预防CHR个体发展为精神病。

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