Recent evidence suggests that Alzheimer’s disease (AD) is closely linked with insulin resistance, as seen in type 2 diabetes mellitus (T2DM). Insulin signaling is impaired in AD brains due to insulin resistance, ultimately resulting in the formation of neurofibrillary tangles (NFTs). AD and T2DM are connected at molecular, clinical, and epidemiological levels making it imperative to understand the contribution of T2DM, and other metabolic disorders, to AD pathogenesis. In this review, we have discussed various modalities involved in the pathogenesis of these two diseases and explained the contributing parameters. Insulin is vital for maintaining glucose homeostasis and it plays an important role in regulating inflammation. Here, we have discussed the roles of various contributing factors like miRNA, leptin hormone, neuroinflammation, metabolic dysfunction, and gangliosides in insulin impairment both in AD and T2DM. Understanding these mechanisms will be a big step forward for making molecular therapies that may help maintain or prevent both AD and T2DM, thus reducing the burden of both these diseases.

最近的证据表明阿尔茨海默病 (AD) 与胰岛素抵抗密切相关，如 2 型糖尿病 (T2DM) 中所见。由于胰岛素抵抗，AD 大脑中的胰岛素信号受损，最终导致神经原纤维缠结 (NFT) 的形成。AD 和 T2DM 在分子、临床和流行病学水平上相互关联，因此必须了解 T2DM 和其他代谢紊乱对 AD 发病机制的贡献。在这篇综述中，我们讨论了涉及这两种疾病发病机制的各种方式，并解释了相关参数。胰岛素对于维持葡萄糖稳态至关重要，并且在调节炎症方面起着重要作用。在这里，我们讨论了各种促成因素的作用，如 miRNA、瘦素激素、神经炎症、AD 和 T2DM 中的代谢功能障碍和胰岛素损伤中的神经节苷脂。了解这些机制将是开发有助于维持或预防 AD 和 T2DM 的分子疗法的一大进步，从而减轻这两种疾病的负担。