摘要
鞘脂类的代谢产生了一些信号分子,深刻影响细胞的增殖,分化和死亡。特别是,一个可用的巨大的身体的信息,它定义了各种角色的神经酰胺和sphingosine-1-phosphate细胞的死亡和生存。本文专门探讨神经酰胺的作用和sphingosine-1 -磷酸在阿尔茨海默氏症引起神经元死亡,通过分析数据和实验研究。有令人信服的证据表明,神经酰胺中发挥着关键作用在发生阿尔茨海默氏症的大脑中的神经细胞退化和amyloidogenesis中。此外,还有另一条神经酰胺和淀粉样β蛋白协调攻击线粒体在细胞死亡的途径。然而,复杂的代谢和信号通路的鞘脂类衍生品排除了立即识别有效的治疗老年痴呆症的药物靶点。
关键词: 鞘磷脂、神经酰胺、Sphingosine-1-phosphate、线粒体淀粉样β蛋白、细胞凋亡、Necroptosis、阿尔茨海默氏症。
Current Alzheimer Research
Title:Ceramide and Sphingosine-1-Phosphate in Cell Death Pathways : Relevance to the Pathogenesis of Alzheimer's Disease
Volume: 13 Issue: 11
Author(s): Sankha Shubhra Chakrabarti, Aritri Bir, Jit Poddar, Maitrayee Sinha, Anirban Ganguly, Sasanka Chakrabarti
Affiliation:
关键词: 鞘磷脂、神经酰胺、Sphingosine-1-phosphate、线粒体淀粉样β蛋白、细胞凋亡、Necroptosis、阿尔茨海默氏症。
摘要: The metabolic turnover of sphingolipids produces several signaling molecules that profoundly affect the proliferation, differentiation and death of cells. In particular, an enormous body of information is available that defines the varied role of ceramide and sphingosine-1-phosphate in cell death and survival. This review specifically examines the role of ceramide and sphingosine-1- phosphate in triggering neuronal death in Alzheimer's disease by analyzing the data from post-mortem studies and experimental research. There is compelling evidence that ceramide plays a key role in the neurodegeneration and amyloidogenesis occurring in the brain in Alzheimer's disease. Further, it appears that ceramide and amyloid beta protein orchestrate an attack on mitochondria to set in the pathways of cell death. However, the complexity of metabolic and signaling pathways of sphingolipid derivatives precludes an immediate identification of effective drug targets for the therapy of Alzheimer's disease.
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Sankha Shubhra Chakrabarti, Aritri Bir, Jit Poddar, Maitrayee Sinha, Anirban Ganguly, Sasanka Chakrabarti , Ceramide and Sphingosine-1-Phosphate in Cell Death Pathways : Relevance to the Pathogenesis of Alzheimer's Disease, Current Alzheimer Research 2016; 13 (11) . https://dx.doi.org/10.2174/1567205013666160603004239
DOI https://dx.doi.org/10.2174/1567205013666160603004239 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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