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阿尔茨海默病中的膜磷脂改变:乙醇胺缩醛磷脂缺乏

Membrane phospholipid alterations in Alzheimer's disease: deficiency of ethanolamine plasmalogens.

作者信息

Farooqui A A, Rapoport S I, Horrocks L A

机构信息

Department of Medical Biochemistry, Ohio State University, Columbus 43210, USA.

出版信息

Neurochem Res. 1997 Apr;22(4):523-7. doi: 10.1023/a:1027380331807.

Abstract

The ethanolamine plasmalogens are decreased whereas serine glycerophospholipids are significantly increased in plasma membrane phospholipid in affected regions of brain in Alzheimer's disease. This may be due to stimulation of Ca(2+)-independent plasmalogen-selective phospholipase A2 which was recently discovered in brain. This phospholipase A2 differs from other Ca(2+)-independent phospholipases A2 in response to ATP and various inhibitors. It may be responsible for excess release of arachidonic acid and accumulation of prostaglandins and lipid peroxides in AD. Accumulation of the above lipid metabolites due to abnormal receptor function and signal transduction may contribute to neurodegeneration in AD.

摘要

在阿尔茨海默病患者大脑的病变区域,乙醇胺缩醛磷脂减少,而丝氨酸甘油磷脂在质膜磷脂中显著增加。这可能是由于最近在大脑中发现的不依赖钙离子的缩醛磷脂选择性磷脂酶A2受到刺激所致。这种磷脂酶A2在对ATP和各种抑制剂的反应方面不同于其他不依赖钙离子的磷脂酶A2。它可能是导致花生四烯酸过度释放以及前列腺素和脂质过氧化物在阿尔茨海默病中积累的原因。由于受体功能和信号转导异常导致上述脂质代谢产物的积累,可能会促使阿尔茨海默病中的神经退行性变。

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