Targeting the Type 5 Metabotropic Glutamate Receptor: A Potential Therapeutic Strategy for Neurodegenerative Diseases?
Targeting the Type 5 Metabotropic Glutamate Receptor: A Potential Therapeutic Strategy for Neurodegenerative Diseases?
复制标题
针对5型代谢型谷氨酸受体：神经退行性疾病的潜在治疗策略？
DOI：
10.3389/fphar.2022.893422
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发表时间：
2022
影响因子：
5.6
通讯作者：
Bradley, Sophie J.
中科院分区：
文献类型：
--
作者：
Budgett, Rebecca F.;Bakker, Geor;Sergeev, Eugenia;Bennett, Kirstie A.;Bradley, Sophie J.
关键词：
5型代谢性谷氨酸受体mGlu5已被认为是治疗几种神经退行性疾病的潜在治疗靶点。在临床前神经退行性疾病模型中，新的变构调节剂已被证明可以改善认知能力并减少疾病相关病理。神经退行性疾病的一个常见病理标志是慢性神经炎症反应，涉及星形胶质细胞和小胶质细胞等胶质细胞。由于mGlu5在星形胶质细胞中表达，靶向这种受体可能提供一种潜在的机制，通过这种机制可以调节神经退行性疾病的神经炎症过程。本综述将讨论当前证据，强调mGlu5变构调节剂治疗神经退行性疾病的潜力，包括阿尔茨海默病、亨廷顿病、帕金森病和肌萎缩性侧索硬化症。此外，本文将探讨mGlu5在神经炎症反应中的作用，以及这种G蛋白偶联受体调节神经炎症的潜力。
The type 5 metabotropic glutamate receptor, mGlu5, has been proposed as a potential therapeutic target for the treatment of several neurodegenerative diseases. In preclinical neurodegenerative disease models, novel allosteric modulators have been shown to improve cognitive performance and reduce disease-related pathology. A common pathological hallmark of neurodegenerative diseases is a chronic neuroinflammatory response, involving glial cells such as astrocytes and microglia. Since mGlu5 is expressed in astrocytes, targeting this receptor could provide a potential mechanism by which neuroinflammatory processes in neurodegenerative disease may be modulated. This review will discuss current evidence that highlights the potential of mGlu5 allosteric modulators to treat neurodegenerative diseases, including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Furthermore, this review will explore the role of mGlu5 in neuroinflammatory responses, and the potential for this G protein-coupled receptor to modulate neuroinflammation.
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影响因子：
4.7
作者：
Biber, K;Laurie, DJ;Boddeke, HWGM
通讯作者：
Boddeke, HWGM
影响因子：
8.6
作者：
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通讯作者：
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DOI：
10.1155/2014/652750
发表时间：
2014
期刊：
ISRN psychiatry
影响因子：
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影响因子：
8.6
作者：
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通讯作者：
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影响因子：
4.7
作者：
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通讯作者：
Basile, AS