cAMP delays beta-amyloid (25-35) induced cell death in rat cortical neurons

被引：15

作者：

Parvathenani, LK ^{[1
]}

Calandra, V ^{[1
]}

Roberts, SB ^{[1
]}

Posmantur, R ^{[1
]}

机构：

[1] Bristol Myers Squibb Co, Pharmaceut Res Inst, GU Neurosci Drug Discovery, Wallingford, CT 06492 USA

来源：

NEUROREPORT | 2000年 / 11卷 / 10期

关键词：

Alzheimer's disease; amyloid beta-peptide; apoptosis; cAMP; caspase-3; neurotoxicity;

D O I：

10.1097/00001756-200007140-00045

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

beta-Amyloid (A beta) accumulation is believed to contribute to neuronal cell death in Alzheimer's disease. To understand the role of cAMP in the regulation of A beta induced cell death, we used 8-chlorophenylthio-cAMP (8-CPT-cAMP, a cAMP anal og) to raise intracellular cAMP levels. Exposure of rat cortical neurons to A beta(25-35) resulted in a gradual increase in lactate dehydrogenase (LDH) over 48 h, which was preceded by a transient elevation in caspase-3-like activity. In the presence of 8CPT-cAMP, both caspase-3 activity and LDH release was significantly reduced. These data suggest that elevation of intracellular cAMP levels attenuate A beta-induced neurotoxicity and may delay or prevent the onset of A beta-induced neurodegeneration. NeuroReport 11:2293-2297 (C) 2000 Lippincott Williams & Wilkins.

引用

页码：2293 / 2297

页数：5

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