Tirzepatide (TRZ) is a dual agonist of glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) receptors that were recently approved for the treatment of type 2 diabetes (T2D) and obesity. Of note is that T2D and obesity, by inducing peripheral low-grade inflammation and oxidative stress, provoke the development of central neuroinflammation and oxidative stress. Together, T2D and obesity are regarded as potential risk factors implicated in the development and progression of Alzheimer's disease (AD), which is the most common neurodegenerative disease and represents the most typical cause of dementia. Hence, targeting low-grade inflammation and oxidative stress in T2D and obesity by TRZ may reduce AD neuropathology. In addition, TRZ can inhibit the production of amyloid beta (Aβ) and associated neuroinflammation, oxidative stress, and neuronal apoptosis. However, the underlying neuroprotective mechanism of TRZ against AD is not entirely explained. Consequently, this mini-review aims to discuss the possible molecular mechanism of TRZ in AD.

Keywords: Alzheimer's disease; Brain insulin signaling; Glucagon-like peptide one and gastric inhibitory polypeptide; Tirzepatide.

© 2025. The Author(s).

特利扎肽（TRZ）是一种胰高血糖素样肽1 (GLP-1) 和胃抑制多肽 (GIP) 受体的双激动剂，最近被批准用于治疗2型糖尿病（T2D）和肥胖症。值得注意的是，2型糖尿病和肥胖通过诱发外周低度炎症和氧化应激，引发中枢神经炎症和氧化应激的发展。总的来说，2型糖尿病和肥胖被视为阿尔茨海默病 (AD) 发展和进展的潜在风险因素，而阿尔茨海默病是最常见的神经退行性疾病，并且是痴呆最常见的原因。因此，通过TRZ靶向2型糖尿病和肥胖中的低度炎症和氧化应激可能减少AD的神经系统病理变化。此外，TRZ可以抑制淀粉样蛋白β（Aβ）的产生及其相关的神经炎症、氧化应激和神经元凋亡。然而，TRZ对抗AD的神经保护机制尚未完全阐明。因此，这篇小型综述旨在讨论TRZ在AD中的可能分子机制。

关键词：阿尔茨海默病；大脑胰岛素信号传导；胰高血糖素样肽一和胃抑制多肽；特利扎肽。

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