期刊
BIOCHEMICAL SOCIETY TRANSACTIONS
卷 32, 期 -, 页码 144-146出版社
PORTLAND PRESS LTD
DOI: 10.1042/BST0320144
关键词
Alzheimer's disease; amyloid-beta peptide; ceramide; lipid peroxidation; tumour necrosis factor alpha (TNF-alpha); sphingomyelin cycle
Alzheimer's disease (AD) is characterized by progressive decline in cognition, memory and intellect. It has been hypothesized that amyloid-beta pepticle (A-beta) may have a prominent role in neurodegeneration. Oxidative mechanisms have been implicated in this pathway, There is substantial evidence that inflammatory mechanisms, induced by tumour necrosis factor alpha (TNF-alpha), are also involved in AD. TNF-alpha activates receptors linked to multiple effector systems, including a sphingomyelin pathway and peroxide oxidation. We have determined the changes of neutral sphingomyelinase activity, sphingomyelin and ceramide contents, and the level of lipid peroxide products (conjugated dienes), in the cerebral cortex, hippocampus and cerebellum of rats within 3 h and 7 days of intracerebral injection of A-beta and TNF-alpha. A single injection of A-beta and TNF-alpha has been shown to increase the level of peroxide products in the hippocampus and cerebral cortex within 3 h and 7 days. Sphingomyelinase activity and ceramide levels have been found to increase 7 days after A-beta administration. We found that activation of the sphingomyelin pathway lies downstream from the oxidative stress.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据