阿尔茨海默病中钙、β-淀粉样蛋白与晚期糖基化终产物受体之间的相互作用。
Crosstalk between calcium, amyloid beta and the receptor for advanced glycation endproducts in Alzheimer's disease.
作者信息
Leclerc Estelle, Sturchler Emmanuel, Vetter Stefan W, Heizmann Claus W
机构信息
Department of Chemistry and Biochemistry, Florida Atlantic University, 777 Glades Road, Boca Raton, FL 33431, USA.
出版信息
Rev Neurosci. 2009;20(2):95-110. doi: 10.1515/revneuro.2009.20.2.95.
Hallmarks of Alzheimer's disease (AD) include the accumulation of amyloid beta peptide (Abeta), hyperphosphorylation of tau protein, and increased inflammatory activity in the hippocampus and cerebral cortex. The receptor for advanced glycation endproducts (RAGE) has been shown to interact with Abeta and to modulate Abeta transport across the blood-brain barrier. Furthermore, RAGE is upregulated at sites of inflammation and its activation results in distinct intracellular signaling cascades in respect to Abeta conformers. Besides Abeta, RAGE interacts with several members of the calcium binding S100 protein family, amphoterin and advanced glycation endproducts. Mounting evidence suggests that RAGE is a key player in the signaling pathways triggered by Abeta and S100 proteins in AD. In this review, we discuss recent discoveries about the crosstalk between RAGE, Abeta and S100 proteins in the pathophysiology of AD.
阿尔茨海默病（AD）的特征包括β淀粉样肽（Aβ）的积累、tau蛋白的过度磷酸化，以及海马体和大脑皮层中炎症活性的增加。晚期糖基化终产物受体（RAGE）已被证明可与Aβ相互作用，并调节Aβ通过血脑屏障的转运。此外，RAGE在炎症部位上调，其激活会导致针对Aβ构象异构体的不同细胞内信号级联反应。除了Aβ，RAGE还与钙结合S100蛋白家族的几个成员、双调蛋白和晚期糖基化终产物相互作用。越来越多的证据表明，RAGE是AD中由Aβ和S100蛋白触发的信号通路中的关键参与者。在这篇综述中，我们讨论了关于RAGE、Aβ和S100蛋白在AD病理生理学中的相互作用的最新发现。
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