Tirzepatide: a novel therapeutic approach for Alzheimer's disease.

IF 3.5 3区医学 Q2 ENDOCRINOLOGY & METABOLISM

Metabolic brain disease Pub Date : 2025-06-11 DOI:10.1007/s11011-025-01649-z

Ghadah H Alshehri, Hayder M Al-Kuraishy, Huda Jaber Waheed, Ali I Al-Gareeb, Safaa A Faheem, Athanasios Alexiou, Marios Papadakis, Gaber El-Saber Batiha

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Abstract

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.

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替西肽：一种治疗阿尔茨海默病的新方法。

Tirzepatide （TRZ）是胰高血糖素样肽1 （GLP-1）和胃抑制多肽（GIP）受体的双重激动剂，最近被批准用于治疗2型糖尿病（T2D）和肥胖。值得注意的是，T2D和肥胖通过诱导周围低度炎症和氧化应激，引起中枢神经炎症和氧化应激的发展。T2D和肥胖一起被认为是阿尔茨海默病（AD）发生和发展的潜在危险因素，AD是最常见的神经退行性疾病，也是痴呆症的最典型原因。因此，通过TRZ靶向T2D和肥胖的低度炎症和氧化应激可能减少AD神经病理。此外，TRZ可以抑制β淀粉样蛋白（Aβ）的产生和相关的神经炎症、氧化应激和神经元凋亡。然而，TRZ对AD的潜在神经保护机制尚未完全解释。因此，本文旨在探讨TRZ在AD中的可能分子机制。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Metabolic brain disease 医学-内分泌学与代谢

CiteScore

5.90

自引率

5.60%

发文量

248

审稿时长

6-12 weeks

期刊介绍： Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.