Roles for dysfunctional sphingolipid metabolism in Alzheimer's disease neuropathogenesis.
Roles for dysfunctional sphingolipid metabolism in Alzheimer's disease neuropathogenesis.
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DOI：
10.1016/j.bbalip.2010.05.003
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发表时间：
2010-08
期刊：
影响因子：
--
通讯作者：
Mattson MP
中科院分区：
文献类型：
--
作者：
Haughey NJ;Bandaru VV;Bae M;Mattson MP
神经细胞膜上的鞘磷脂通过调节膜相关受体的定位和激活，或作为生物活性脂质介质的前体，在信号转导中发挥重要作用。细胞因子和神经营养因子受体与鞘磷脂酶偶联，激活后产生神经酰胺和神经节苷脂，进而改变神经元的结构和功能可塑性。在衰老和神经退行性疾病中，如阿尔茨海默病(AD)，膜相关的氧化应激增加，神经酰胺的过度产生和积累。对人类受试者的脑组织样本和这些疾病的实验模型的研究表明，神经鞘磷脂代谢紊乱是阿尔茨海默病和艾滋病毒痴呆症神经元功能障碍和退化的关键事件。针对鞘磷脂代谢的饮食和药物干预应用于预防和治疗神经退行性疾病。
Sphingolipids in the membranes of neurons play important roles in signal transduction, either by modulating the localization and activation of membrane-associated receptors or by acting as precursors of bioactive lipid mediators. Activation of cytokine and neurotrophic factor receptors coupled to sphingomyelinases results in the generation of ceramides and gangliosides, which in turn, modify the structural and functional plasticity of neurons. In aging and neurodegenerative conditions such as Alzheimer’s disease (AD), there is increased membrane-associated oxidative stress and excessive production and accumulation of ceramides. Studies of brain tissue samples from human subjects, and of experimental models of the diseases, suggest that perturbed sphingomyelin metabolism is a pivotal event in the dysfunction and degeneration of neurons that occurs in AD and HIV dementia. Dietary and pharmacological interventions that target sphingolipid metabolism should be pursued for the prevention and treatment of neurodegenerative disorders.
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