Changes in insulin and insulin signaling in Alzheimer's disease: cause or consequence?
Changes in insulin and insulin signaling in Alzheimer's disease: cause or consequence?
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DOI：
10.1084/jem.20160493
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发表时间：
2016-07-25
期刊：
影响因子：
--
通讯作者：
Holtzman DM
中科院分区：
文献类型：
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作者：
Stanley M;Macauley SL;Holtzman DM
Stanley及其同事探讨了胰岛素水平和胰岛素信号的变化是否是AD的原因或结果。2型糖尿病患者患阿尔茨海默病（AD）的风险增加，尽管因果关系仍然知之甚少。在AD脑中报告了胰岛素信号传导（IS）的改变。此外，淀粉样蛋白-β（Aβ）的寡聚体/纤维可导致神经元胰岛素抵抗，并且鼻内胰岛素正被探索作为AD的潜在治疗。相反，在AD患者中发现胰岛素水平（ins）升高，并且已报告高胰岛素会增加Aβ水平和tau磷酸化，这可能加剧AD病理。在此，我们探讨是否在ins和IS的变化是AD的原因或后果。
Stanley and colleagues explore whether changes in insulin levels and insulin signaling are a cause or consequence of AD. Individuals with type 2 diabetes have an increased risk for developing Alzheimer’s disease (AD), although the causal relationship remains poorly understood. Alterations in insulin signaling (IS) are reported in the AD brain. Moreover, oligomers/fibrils of amyloid-β (Aβ) can lead to neuronal insulin resistance and intranasal insulin is being explored as a potential therapy for AD. Conversely, elevated insulin levels (ins) are found in AD patients and high insulin has been reported to increase Aβ levels and tau phosphorylation, which could exacerbate AD pathology. Herein, we explore whether changes in ins and IS are a cause or consequence of AD.