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神经肽作为神经疾病治疗药物的潜力。

Potentials of Neuropeptides as Therapeutic Agents for Neurological Diseases.

作者信息

Yeo Xin Yi, Cunliffe Grace, Ho Roger C, Lee Su Seong, Jung Sangyong

机构信息

Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), Singapore 138667, Singapore.

Department of Psychological Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228, Singapore.

出版信息

Biomedicines. 2022 Feb 1;10(2):343. doi: 10.3390/biomedicines10020343.

Abstract

Despite recent leaps in modern medicine, progress in the treatment of neurological diseases remains slow. The near impermeable blood-brain barrier (BBB) that prevents the entry of therapeutics into the brain, and the complexity of neurological processes, limits the specificity of potential therapeutics. Moreover, a lack of etiological understanding and the irreversible nature of neurological conditions have resulted in low tolerability and high failure rates towards existing small molecule-based treatments. Neuropeptides, which are small proteinaceous molecules produced by the body, either in the nervous system or the peripheral organs, modulate neurological function. Although peptide-based therapeutics originated from the treatment of metabolic diseases in the 1920s, the adoption and development of peptide drugs for neurological conditions are relatively recent. In this review, we examine the natural roles of neuropeptides in the modulation of neurological function and the development of neurological disorders. Furthermore, we highlight the potential of these proteinaceous molecules in filling gaps in current therapeutics.

摘要

尽管现代医学最近取得了飞跃,但神经疾病的治疗进展仍然缓慢。几乎不可渗透的血脑屏障(BBB)阻止治疗药物进入大脑,以及神经过程的复杂性,限制了潜在治疗药物的特异性。此外,对病因的认识不足以及神经疾病的不可逆性导致对现有的基于小分子的治疗方法耐受性低且失败率高。神经肽是身体在神经系统或外周器官中产生的小蛋白质分子,可调节神经功能。尽管基于肽的治疗方法起源于20世纪20年代对代谢疾病的治疗,但用于神经疾病的肽药物的采用和开发相对较新。在这篇综述中,我们研究了神经肽在调节神经功能和神经疾病发展中的天然作用。此外,我们强调了这些蛋白质分子在填补当前治疗空白方面的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed21/8961788/6d7d3865d249/biomedicines-10-00343-g001.jpg

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