Stanley Molly, Macauley Shannon L, Holtzman David M
Department of Neurology, Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO.
Department of Neurology, Hope Center for Neurological Disorders, Charles F. and Joanne Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO
J Exp Med. 2016 Jul 25;213(8):1375-85. doi: 10.1084/jem.20160493. Epub 2016 Jul 18.
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.
2型糖尿病患者患阿尔茨海默病（AD）的风险增加，尽管其因果关系仍知之甚少。据报道，AD大脑中存在胰岛素信号传导（IS）改变。此外，淀粉样β蛋白（Aβ）的寡聚体/原纤维可导致神经元胰岛素抵抗，鼻内胰岛素正作为AD的一种潜在治疗方法进行研究。相反，AD患者体内胰岛素水平（ins）升高，据报道高胰岛素会增加Aβ水平和tau蛋白磷酸化，这可能会加剧AD病理。在此，我们探讨ins和IS的变化是AD的原因还是结果。
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