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Linking Alzheimer’s Disease and Type 2 Diabetes Mellitus via Aberrant Insulin Signaling and Inflammation

机译:通过异常的胰岛素信号传导和炎症联系阿尔茨海默氏病和2型糖尿病

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摘要

Alzheimer’s disease (AD) and type 2 diabetes mellitus (T2DM) are two progressive and devastating health disorders afflicting millions of people worldwide. The probability and incidence of both have increased considerably in recent years consequent to increased longevity and population growth. Progressively more links are being continuously found between inflammation and central nervous system disorders like AD, Parkinson's disease, Huntington's disease, motor neuron disease, multiple sclerosis, stroke, traumatic brain injury and even cancers of the nervous tissue. The depth of the relationship depends on the timing and extent of anti- or pro-inflammatory gene expression. Inflammation has also been implicated in T2DM. Misfolding and fibrillization (of tissue specific and/or non-specific proteins) are features common to both AD and T2DM and are induced by as well as contribute to inflammation and stress (oxidative/glycation). This review appraises the roles of inflammation and abnormalities in the insulin signaling system as important shared features of T2DM and AD. The capacity of anti-cholinesterases in reducing the level of certain common inflammatory markers in particular if they may provide therapeutic potential to mitigate awry mechanisms leading to AD.
机译:阿尔茨海默氏病(AD)和2型糖尿病(T2DM)是两种进行性和破坏性的健康疾病,困扰着全球数百万人。由于寿命的延长和人口的增长,近年来两者的发生率和发生率都大大增加了。在炎症和中枢神经系统疾病(例如AD,帕金森氏病,亨廷顿氏病,运动神经元疾病,多发性硬化症,中风,脑外伤甚至神经组织癌症)之间,越来越多的联系正在不断发现。关系的深度取决于抗炎或促炎基因表达的时机和程度。炎症也与T2DM有关。 (组织特异性和/或非特异性蛋白的)错误折叠和原纤维化是AD和T2DM共同的特征,并且由炎症和应激(氧化/糖基化)诱导并促成。这篇综述评估了炎症和异常在胰岛素信号系统中的作用,将其作为T2DM和AD的重要共享特征。抗胆碱酯酶降低某些常见炎症标记物水平的能力,特别是如果它们可提供治疗潜力以减轻导致AD的不良机制时,尤其如此。

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