Astrocytes are the homeostatic and protective cells of the central nervous system (CNS). In neurological diseases, astrocytes undergo complex changes, which are subclassified into (1) reactive astrogliosis, an evolutionary conserved defensive rearrangement of cellular phenotype aimed at neuroprotection; (2) pathological remodeling, when astrocytes acquire new features driving pathology; and (3) astrodegeneration, which is manifested by astroglial atrophy and loss of homeostatic functions. In aging brains as well as in the brains affected by Alzheimer's disease (AD), astrocytes acquire both atrophic and reactive phenotypes in a region- and disease-stage-dependent manner. Prevalence of atrophy overreactivity, observed in certain brain regions and in terminal stages of the disease, arguably facilitates the development of neurological deficits. Astrocytes exhibit ionic excitability mediated by changes in intracellular concentration of ions, most importantly of Ca2+ and Na+, with intracellular ion dynamics triggered by the activity of neural networks. AD astrocytes associated with senile plaques demonstrate Ca2+ hyperactivity in the form of aberrant Ca2+ oscillations and pathological long-range Ca2+ waves. Astroglial Ca2+ signaling originating from Ca2+ release from the endoplasmic reticulum is a key factor in initiating astrogliotic response; deficient Ca2+ signaling toolkits observed in entorhinal and prefrontal cortices of AD model animals may account for vulnerability of these regions to the pathology.

中文翻译：

---

星形胶质细胞钙信号在衰老和阿尔茨海默病中的作用。

星形胶质细胞是中枢神经系统 (CNS) 的稳态和保护细胞。在神经系统疾病中，星形胶质细胞经历复杂的变化，这些变化被细分为 (1) 反应性星形胶质细胞增生症，一种旨在保护神经的细胞表型的进化保守防御重排；(2)病理重塑，当星形胶质细胞获得驱动病理的新特征时；(3) 星形变性，表现为星形胶质细胞萎缩和稳态功能丧失。在老化的大脑以及受阿尔茨海默病 (AD) 影响的大脑中，星形胶质细胞以区域和疾病阶段依赖性方式获得萎缩和反应性表型。在某些大脑区域和疾病的晚期阶段观察到的萎缩过度反应的流行可以说促进了神经功能缺陷的发展。星形胶质细胞表现出由细胞内离子浓度变化介导的离子兴奋性，最重要的是 Ca2+ 和 Na+，细胞内离子动力学由神经网络的活动触发。与老年斑相关的 AD 星形胶质细胞表现出异常 Ca2+ 振荡和病理性长程 Ca2+ 波形式的 Ca2+ 过度活跃。源自内质网 Ca2+ 释放的星形胶质细胞 Ca2+ 信号是启动星形胶质细胞反应的关键因素；在 AD 模型动物的内嗅和前额叶皮质中观察到的 Ca2+ 信号传导工具包缺陷可能是这些区域对病理的脆弱性的原因。具有由神经网络活动触发的细胞内离子动力学。与老年斑相关的 AD 星形胶质细胞表现出异常 Ca2+ 振荡和病理性长程 Ca2+ 波形式的 Ca2+ 过度活跃。源自内质网 Ca2+ 释放的星形胶质细胞 Ca2+ 信号是启动星形胶质细胞反应的关键因素；在 AD 模型动物的内嗅和前额叶皮质中观察到的 Ca2+ 信号传导工具包缺陷可能是这些区域对病理的脆弱性的原因。具有由神经网络活动触发的细胞内离子动力学。与老年斑相关的 AD 星形胶质细胞表现出异常 Ca2+ 振荡和病理性长程 Ca2+ 波形式的 Ca2+ 过度活跃。源自内质网 Ca2+ 释放的星形胶质细胞 Ca2+ 信号是启动星形胶质细胞反应的关键因素；在 AD 模型动物的内嗅和前额叶皮质中观察到的 Ca2+ 信号传导工具包缺陷可能是这些区域对病理的脆弱性的原因。