Glutamate, the major excitatory neurotransmitter in the brain exerts its effects via both ionotropic glutamate receptors and metabotropic glutamate receptors (mGluRs). There are three subgroups of mGluRs, pre-synaptic Group II and Group III mGluRs and post-synaptic Group I mGluRs. mGluRs are ubiquitously expressed in the brain and their activation is poised upstream of a myriad of signaling pathways, resulting in their implication in the pathogenesis of various neurodegenerative diseases including, Alzheimer’s Disease (AD). While the exact mechanism of AD etiology remains elusive, β-amyloid (Aβ) plaques and hyperphosphorylated tau tangles remain the histopathological hallmarks of AD. Though less electrically excitable, neuroglia are a major non-neuronal cell type in the brain and are composed of astrocytes, microglia, and oligodendrocytes. Astrocytes, microglia, and oligodendrocytes provide structural and metabolic support, active immune defence, and axonal support and sheathing, respectively. Interestingly, Aβ and hyperphosphorylated tau are known to disrupt the neuroglial homeostasis in the brain, pushing them towards a more neurotoxic state. In this review, we discuss what is currently known regarding the expression patterns of various mGluRs in neuroglia and how Aβ and tau alter the normal mGluR function in the neuroglia and contribute to the pathophysiology of AD.

中文翻译：

---

神经胶质代谢型谷氨酸受体在阿尔茨海默病中的作用

谷氨酸是大脑中主要的兴奋性神经递质，它通过离子型谷氨酸受体和代谢型谷氨酸受体 (mGluR) 发挥作用。mGluRs 分为三个亚组：突触前第 II 组和第 III 组 mGluRs 以及突触后第 I 组 mGluRs。mGluRs 在大脑中普遍表达，它们的激活处于无数信号通路的上游，导致它们参与各种神经退行性疾病（包括阿尔茨海默氏病 (AD)）的发病机制。虽然 AD 病因学的确切机制仍然难以捉摸，但 β-淀粉样蛋白 (Aβ) 斑块和过度磷酸化的 tau 蛋白缠结仍然是 AD 的组织病理学标志。虽然电兴奋性较低，但神经胶质细胞是大脑中主要的非神经元细胞类型，由星形胶质细胞、小胶质细胞和少突胶质细胞组成。星形胶质细胞、小胶质细胞和少突胶质细胞分别提供结构和代谢支持、主动免疫防御以及轴突支持和护套。有趣的是，已知 Aβ 和过度磷酸化的 tau 会破坏大脑中的神经胶质细胞稳态，将它们推向更具神经毒性的状态。在这篇综述中，我们讨论了目前已知的关于神经胶质细胞中各种 mGluR 表达模式的知识，以及 Aβ 和 tau 如何改变神经胶质细胞中正常的 mGluR 功能并促进 AD 的病理生理学。