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氯胺酮和锌:通过双重 NMDA 受体调节治疗神经性厌食症。

Ketamine and Zinc: Treatment of Anorexia Nervosa Via Dual NMDA Receptor Modulation.

机构信息

Thompson Institute, University of the Sunshine Coast, 12 Innovations Parkway, Birtinya, 4575, Sunshine Coast, QLD, Australia.

Brain & Mind Research Centre, University of Sydney, Sydney, NSW, Australia.

出版信息

CNS Drugs. 2023 Feb;37(2):159-180. doi: 10.1007/s40263-022-00984-4. Epub 2023 Jan 22.

Abstract

Anorexia nervosa is a disorder associated with serious adverse health outcomes, for which there is currently considerable treatment ineffectiveness. Characterised by restrictive eating behaviours, distorted body image perceptions and excessive physical activity, there is growing recognition anorexia nervosa is associated with underlying dysfunction in excitatory and inhibitory neurometabolite metabolism and signalling. This narrative review critically explores the role of N-methyl-D-aspartate receptor-mediated excitatory and inhibitory neurometabolite dysfunction in anorexia nervosa and its associated biomarkers. The existing magnetic resonance spectroscopy literature in anorexia nervosa is reviewed and we outline the brain region-specific neurometabolite changes that have been reported and their connection to anorexia nervosa psychopathology. Considering the proposed role of dysfunctional neurotransmission in anorexia nervosa, the potential utility of zinc supplementation and sub-anaesthetic doses of ketamine in normalising this is discussed with reference to previous research in anorexia nervosa and other neuropsychiatric conditions. The rationale for future research to investigate the combined use of low-dose ketamine and zinc supplementation to potentially extend the therapeutic benefits in anorexia nervosa is subsequently explored and promising biological markers for assessing and potentially predicting treatment response are outlined.

摘要

神经性厌食症是一种与严重不良健康后果相关的疾病,目前其治疗效果并不理想。这种疾病的特征是限制进食行为、身体形象感知扭曲和过度的身体活动,越来越多的人认识到,神经性厌食症与兴奋性和抑制性神经代谢物代谢和信号传导的潜在功能障碍有关。本综述批判性地探讨了 N-甲基-D-天冬氨酸受体介导的兴奋性和抑制性神经代谢物功能障碍在神经性厌食症及其相关生物标志物中的作用。本文回顾了神经性厌食症的现有磁共振波谱研究,并概述了已报道的与神经性厌食症精神病学相关的特定脑区神经代谢物变化。考虑到神经传递功能障碍在神经性厌食症中的作用,本文还讨论了锌补充剂和亚麻醉剂量氯胺酮在使这种功能正常化方面的潜在效用,并参考了神经性厌食症和其他神经精神疾病的先前研究。随后探讨了未来研究联合使用低剂量氯胺酮和锌补充剂以潜在扩大神经性厌食症治疗益处的合理性,并概述了用于评估和潜在预测治疗反应的有前途的生物学标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d4d/9911496/ea24113a9057/40263_2022_984_Fig1_HTML.jpg

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