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嘌呤能受体在阿尔茨海默病中的治疗潜力及有前景的治疗调节剂。

The Therapeutic Potential of Purinergic Receptors in Alzheimer's Disease and Promising Therapeutic Modulators.

机构信息

Department of Nuclear Medicine, Laboratory of Clinical Nuclear Medicine, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, China.

Thyroid and Parethyroid Surgery Center, West China Hospital, Sichuan University, China.

出版信息

Mini Rev Med Chem. 2021;21(11):1288-1302. doi: 10.2174/1389557520999201209211610.

DOI:10.2174/1389557520999201209211610
PMID:33302833
Abstract

Recent studies have proven that the purinergic signaling pathway plays a key role in neurotransmission and neuromodulation, and is involved in various neurodegenerative diseases and psychiatric disorders. With the characterization of the subtypes of receptors in purinergic signaling, i.e. the P1 (adenosine), P2X (ion channel) and P2Y (G protein-coupled), more attention has been paid to the pathophysiology and therapeutic potential of purinergic signaling in the central nervous system disorders. Alzheimer's disease (AD) is a progressive and deadly neurodegenerative disease that is characterized by memory loss, cognitive impairment and dementia. However, as drug development aimed to prevent or control AD has series of failures in recent years, more researchers have focused on the neuroprotection-related mechanisms such as purinergic signaling in AD patients to find a potential cure. This article reviews the recent discoveries of purinergic signaling in AD, and summarizes the potential agents as modulators for the receptors of purinergic signaling in AD-related research and treatments. Thus, our paper provides an insight into purinergic signaling in the development of anti- AD therapies.

摘要

最近的研究已经证明,嘌呤能信号通路在神经传递和神经调节中起着关键作用,并且与各种神经退行性疾病和精神障碍有关。随着嘌呤能信号转导中受体亚型的表征,即 P1(腺苷)、P2X(离子通道)和 P2Y(G 蛋白偶联),人们更加关注嘌呤能信号在中枢神经系统疾病中的病理生理学和治疗潜力。阿尔茨海默病(AD)是一种进行性和致命的神经退行性疾病,其特征是记忆力减退、认知障碍和痴呆。然而,由于近年来旨在预防或控制 AD 的药物开发屡屡失败,更多的研究人员关注 AD 患者的神经保护相关机制,如嘌呤能信号转导,以寻找潜在的治疗方法。本文综述了嘌呤能信号在 AD 中的最新发现,并总结了作为 AD 相关研究和治疗中嘌呤能信号转导受体调节剂的潜在药物。因此,我们的论文深入探讨了嘌呤能信号在抗 AD 治疗中的作用。

相似文献

1
The Therapeutic Potential of Purinergic Receptors in Alzheimer's Disease and Promising Therapeutic Modulators.嘌呤能受体在阿尔茨海默病中的治疗潜力及有前景的治疗调节剂。
Mini Rev Med Chem. 2021;21(11):1288-1302. doi: 10.2174/1389557520999201209211610.
2
Introduction to the Special Issue on Purinergic Receptors.嘌呤能受体专刊介绍
Adv Exp Med Biol. 2017;1051:1-6. doi: 10.1007/5584_2017_12.
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Purinergic signaling in Alzheimer's disease.嘌呤能信号在阿尔茨海默病中的作用。
Brain Res Bull. 2019 Sep;151:25-37. doi: 10.1016/j.brainresbull.2018.10.014. Epub 2018 Nov 22.
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Tackling Chronic Pain and Inflammation through the Purinergic System.通过嘌呤能系统治疗慢性疼痛和炎症。
Curr Med Chem. 2018;25(32):3830-3865. doi: 10.2174/0929867324666170710110630.
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Purinergic Signalling and Neurological Diseases: An Update.嘌呤能信号转导与神经退行性疾病:研究进展
CNS Neurol Disord Drug Targets. 2017;16(3):257-265. doi: 10.2174/1871527315666160922104848.
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Purinergic Receptors Crosstalk with CCR5 to Amplify Ca Signaling.嘌呤能受体与 CCR5 相互作用放大 Ca 信号。
Cell Mol Neurobiol. 2021 Jul;41(5):1085-1101. doi: 10.1007/s10571-020-01002-1. Epub 2020 Nov 20.
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Approaches for designing and discovering purinergic drugs for gastrointestinal diseases.用于设计和发现治疗胃肠道疾病的嘌呤能药物的方法。
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More purinergic receptors deserve attention as therapeutic targets for the treatment of cardiovascular disease.更多嘌呤能受体值得作为心血管疾病治疗的治疗靶点引起关注。
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P2X receptors as drug targets.P2X 受体作为药物靶点。
Mol Pharmacol. 2013 Apr;83(4):759-69. doi: 10.1124/mol.112.083758. Epub 2012 Dec 19.
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Targeting Purinergic Signaling and Cell Therapy in Cardiovascular and Neurodegenerative Diseases.靶向嘌呤能信号和细胞疗法治疗心血管和神经退行性疾病。
Adv Exp Med Biol. 2019;1201:275-353. doi: 10.1007/978-3-030-31206-0_14.

引用本文的文献

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Purinergic Receptor (P2X7R): A Promising Anti-Parkinson's Drug Target.嘌呤能受体(P2X7R):一个有前景的抗帕金森病药物靶点。
Adv Pharm Bull. 2024 Dec 30;14(4):807-818. doi: 10.34172/apb.43206. Epub 2024 Dec 18.
2
Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.阿尔茨海默病是人类大脑自然老化的固有组成部分:综合视角。
Free Neuropathol. 2022 Jul 8;3:17. doi: 10.17879/freeneuropathology-2022-3806. eCollection 2022 Jan.