Ali Naif H, Al-Kuraishy Hayder M, Al-Gareeb Ali I, Alexiou Athanasios, Papadakis Marios, Bahaa Mostafa M, Alibrahim Fawaz, Batiha Gaber El-Saber
Department of Internal Medicine, Medical College, Najran University, Najran, Saudi Arabia.
Department of Clinical pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
J Cell Mol Med. 2024 Dec;28(23):e70118. doi: 10.1111/jcmm.70118.
The metabolic syndrome or syndrome X is a clustering of different components counting insulin resistance (IR), glucose intolerance, visceral obesity, hypertension and dyslipidemia. It has been shown that IR and dysregulation of insulin signalling play a critical role in the development of metabolic syndrome by initiating the pathophysiology of metabolic syndrome through induction of glucolipotoxicity, impairment of glucose disposal and triggering of pro-inflammatory response. Furthermore, metabolic syndrome unfavourably affects the cognitive function and the development of different neurodegenerative diseases such as Alzheimer disease (AD) by inducing oxidative stress, neuroinflammation and brain IR. These changes together with brain IR impair cerebrovascular reactivity leading to cognitive impairment. In addition, metabolic syndrome increases the risk for the development of AD. However, the central mechanisms by which metabolic syndrome amplify AD risk are not completely elucidated. Consequently, this narrative review aims to revise from published articles the association between metabolic syndrome and AD regarding cellular and subcellular pathways. In conclusion, metabolic syndrome is regarded as a potential risk factor for the induction of AD neuropathology by different signalling pathways such as initiation of brain IR, activation of inflammatory signalling pathways and neuroinflammation.
代谢综合征或X综合征是一组不同组分的聚集，包括胰岛素抵抗（IR）、葡萄糖耐量异常、内脏肥胖、高血压和血脂异常。研究表明，胰岛素抵抗和胰岛素信号传导失调在代谢综合征的发生发展中起关键作用，通过诱导糖脂毒性、损害葡萄糖代谢以及引发促炎反应启动代谢综合征的病理生理学过程。此外，代谢综合征通过诱导氧化应激、神经炎症和脑胰岛素抵抗，对认知功能以及不同神经退行性疾病如阿尔茨海默病（AD）的发展产生不利影响。这些变化与脑胰岛素抵抗一起损害脑血管反应性，导致认知障碍。此外，代谢综合征增加了患AD的风险。然而，代谢综合征增加AD风险的核心机制尚未完全阐明。因此，本叙述性综述旨在从已发表的文章中回顾代谢综合征与AD在细胞和亚细胞途径方面的关联。总之，代谢综合征被认为是通过不同信号通路（如脑胰岛素抵抗的启动、炎症信号通路的激活和神经炎症）诱导AD神经病理学的潜在危险因素。
