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The CCAAT/enhancer binding protein (C/EBP) δ is differently regulated by fibrillar and oligomeric forms of the Alzheimer amyloid-β peptide

机译:CCAAT /增强子结合蛋白(C / EBP)δ受Alzheimer淀粉样β肽的原纤维和寡聚形式的不同调节

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摘要

BackgroundThe transcription factors CCAAT/enhancer binding proteins (C/EBP) α, β and δ have been shown to be expressed in brain and to be involved in regulation of inflammatory genes in concert with nuclear factor κB (NF-κB). In general, C/EBPα is down-regulated, whereas both C/EBPβ and δ are up-regulated in response to inflammatory stimuli. In Alzheimer's disease (AD) one of the hallmarks is chronic neuroinflammation mediated by astrocytes and microglial cells, most likely induced by the formation of amyloid-β (Aβ) deposits. The inflammatory response in AD has been ascribed both beneficial and detrimental roles. It is therefore important to delineate the inflammatory mediators and signaling pathways affected by Aβ deposits with the aim of defining new therapeutic targets.
机译:背景已证明转录因子CCAAT /增强子结合蛋白(C / EBP)α,β和δ在脑中表达,并与核因子κB(NF-κB)一起参与炎症基因的调控。通常,响应于炎症刺激,C /EBPα被下调,而C /EBPβ和δ都被上调。在阿尔茨海默氏病(AD)中,标志之一是由星形胶质细胞和小胶质细胞介导的慢性神经炎症,最有可能是由淀粉样β(Aβ)沉积物形成的。 AD中的炎症反应被认为是有益的和有害的作用。因此,重要的是要描述受Aβ沉积物影响的炎症介质和信号传导途径,以期确定新的治疗靶标。

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