摘要
星型胶质细胞的病理重塑代表了阿尔兹海默病(AD)中一种重要的病理成分,阿尔兹海默病胶质细胞经历了萎缩和反应,使得疾病的演化过程中不同阶段更加的具体。星性胶质细胞反应代表了普遍的防御机制,胶质细胞反应抑制剂加剧了β-淀粉样蛋白与AD相连的病理机制。在AD动物模型中,星形胶质细胞在不同脑区域的活性是不同的,嗅皮质和前额叶皮质中观察到的反应活性空白可能与AD过程易损性有关。星形胶质细胞活性与星形胶质细胞内 Ca2+信号有联系,后者被广泛认为是星形胶质细胞兴奋性的机制。在动物模型中的AD病理以及急性和慢性β-淀粉样蛋白的暴露诱导了星性胶质细胞中钙通道程序的病理重塑,这种重塑调整了星性胶质细胞钙信号通路并有可能与AD病理的细胞基质有联系。
关键词: 阿尔茨海默病;星形胶质细胞;星形胶质细胞萎缩;胶质增生;钙信号转导;谷氨酸受体;InsP3受体;神经胶质细胞;β-淀粉样蛋白
Current Alzheimer Research
Title:Calcium Signalling Toolkits in Astrocytes and Spatio-Temporal Progression of Alzheimer's Disease
Volume: 13 Issue: 4
Author(s): Dmitry Lim, J.J Rodriguez-Arellano, Vladimir Parpura, Robert Zorec, Fares Zeidan-Chulia, Armando A. Genazzani and Alexei Verkhratsky
Affiliation:
关键词: 阿尔茨海默病;星形胶质细胞;星形胶质细胞萎缩;胶质增生;钙信号转导;谷氨酸受体;InsP3受体;神经胶质细胞;β-淀粉样蛋白
摘要: Pathological remodelling of astroglia represents an important component of the pathogenesis of Alzheimer's disease (AD). In AD astrocytes undergo both atrophy and reactivity; which may be specific for different stages of the disease evolution. Astroglial reactivity represents the generic defensive mechanism, and inhibition of astrogliotic response exacerbates b-amyloid pathology associated with AD. In animal models of AD astroglial reactivity is different in different brain regions, and the deficits of reactive response observed in entorhinal and prefrontal cortices may be linked to their vulnerability to AD progression. Reactive astrogliosis is linked to astroglial Ca2+ signalling, this latter being widely regarded as a mechanism of astroglial excitability. The AD pathology evolving in animal models as well as acute or chronic exposure to β-amyloid induce pathological remodelling of Ca2+ signalling toolkit in astrocytes. This remodelling modifies astroglial Ca2+ signalling and may be linked to cellular mechanisms of AD pathogenesis.
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Dmitry Lim, J.J Rodriguez-Arellano, Vladimir Parpura, Robert Zorec, Fares Zeidan-Chulia, Armando A. Genazzani and Alexei Verkhratsky , Calcium Signalling Toolkits in Astrocytes and Spatio-Temporal Progression of Alzheimer's Disease, Current Alzheimer Research 2016; 13 (4) . https://dx.doi.org/10.2174/1567205013666151116130104
DOI https://dx.doi.org/10.2174/1567205013666151116130104 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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