Department of Neurology and Alzheimer's Disease Center, University of Kansas Medical Center, Fairway, KS 66205, USA.
Curr Neurol Neurosci Rep. 2012 Oct;12(5):520-7. doi: 10.1007/s11910-012-0297-0.
Accumulating evidence indicates a role for metabolic dysfunction in the pathogenesis of Alzheimer's disease (AD). It is widely reported that Type 2 diabetes (T2D) increases the risk of developing AD, and several postmortem analyses have found evidence of insulin resistance in the AD brain. Thus, insulin-based therapies have emerged as potential strategies to slow cognitive decline in AD. The main methods for targeting insulin to date have been intravenous insulin infusion, intranasal insulin administration, and use of insulin sensitizers. These methods have elicited variable results regarding improvement in cognitive function. This review will discuss the rationale for targeting insulin signaling to improve cognitive function in AD, the results of clinical studies that have targeted insulin signaling, and what these results mean for future studies of the role of insulin-based therapies for AD.
越来越多的证据表明代谢功能障碍在阿尔茨海默病（AD）的发病机制中起作用。据广泛报道，2 型糖尿病（T2D）会增加患 AD 的风险，并且几项尸检分析发现 AD 大脑中存在胰岛素抵抗的证据。因此，基于胰岛素的疗法已成为减缓 AD 认知衰退的潜在策略。迄今为止，针对胰岛素的主要方法是静脉内胰岛素输注、鼻内胰岛素给药和使用胰岛素增敏剂。这些方法在改善认知功能方面取得了不同的结果。这篇综述将讨论针对胰岛素信号改善 AD 认知功能的基本原理、针对胰岛素信号的临床研究结果，以及这些结果对 AD 中基于胰岛素的治疗作用的未来研究意味着什么。
