Obesity-induced neuronal senescence: Unraveling the pathophysiological links

IF 12.5 1区医学 Q1 CELL BIOLOGY

Ageing Research Reviews Pub Date : 2024-10-03 DOI:10.1016/j.arr.2024.102533

Puja Ghosh , Rosaria Anna Fontanella , Lucia Scisciola , Fatemeh Taktaz , Ada Pesapane , Manuela Giovanna Basilicata , Giovanni Tortorella , Giulia Matacchione , Annalisa Capuano , Maria Teresa Vietri , Francesco Selvaggi , Giuseppe Paolisso , Michelangela Barbieri

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Abstract

Obesity is one of the most prevalent and increasing metabolic disorders and is considered one of the twelve risk factors for dementia. Numerous studies have demonstrated that obesity induces pathophysiological changes leading to cognitive decline; however, the underlying molecular mechanisms are yet to be fully elucidated. Various biochemical processes, including chronic inflammation, oxidative stress, insulin resistance, dysregulation of lipid metabolism, disruption of the blood-brain barrier, and the release of adipokines have been reported to contribute to the accumulation of senescent neurons during obesity. These senescent cells dysregulate neuronal health and function by exhibiting a senescence-associated secretory phenotype, inducing neuronal inflammation, deregulating cellular homeostasis, causing mitochondrial dysfunction, and promoting microglial infiltration. These factors act as major risks for the occurrence of neurodegenerative diseases and cognitive decline. This review aims to focus on how obesity upregulates neuronal senescence and explores both pharmacological and non-pharmacological interventions for preventing cognitive impairments, thus offering new insights into potential therapeutic strategies.

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肥胖诱导的神经元衰老：揭开病理生理学的联系。

肥胖症是最普遍且日益严重的代谢性疾病之一，被认为是痴呆症的十二个危险因素之一。大量研究表明，肥胖会诱发导致认知能力下降的病理生理变化；然而，其潜在的分子机制尚未完全阐明。据报道，各种生化过程，包括慢性炎症、氧化应激、胰岛素抵抗、脂质代谢失调、血脑屏障破坏和脂肪因子的释放，都是肥胖导致衰老神经元积累的原因。这些衰老细胞表现出与衰老相关的分泌表型，诱发神经元炎症，破坏细胞稳态，导致线粒体功能障碍，并促进小胶质细胞浸润，从而使神经元的健康和功能失调。这些因素是导致神经退行性疾病和认知能力下降的主要危险因素。本综述旨在关注肥胖如何上调神经元衰老，并探讨预防认知障碍的药物和非药物干预措施，从而为潜在的治疗策略提供新的见解。

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

Ageing Research Reviews 医学-老年医学

CiteScore

19.80

自引率

2.30%

发文量

216

审稿时长

55 days

期刊介绍： With the rise in average human life expectancy, the impact of ageing and age-related diseases on our society has become increasingly significant. Ageing research is now a focal point for numerous laboratories, encompassing leaders in genetics, molecular and cellular biology, biochemistry, and behavior. Ageing Research Reviews (ARR) serves as a cornerstone in this field, addressing emerging trends. ARR aims to fill a substantial gap by providing critical reviews and viewpoints on evolving discoveries concerning the mechanisms of ageing and age-related diseases. The rapid progress in understanding the mechanisms controlling cellular proliferation, differentiation, and survival is unveiling new insights into the regulation of ageing. From telomerase to stem cells, and from energy to oxyradical metabolism, we are witnessing an exciting era in the multidisciplinary field of ageing research. The journal explores the cellular and molecular foundations of interventions that extend lifespan, such as caloric restriction. It identifies the underpinnings of manipulations that extend lifespan, shedding light on novel approaches for preventing age-related diseases. ARR publishes articles on focused topics selected from the expansive field of ageing research, with a particular emphasis on the cellular and molecular mechanisms of the aging process. This includes age-related diseases like cancer, cardiovascular disease, diabetes, and neurodegenerative disorders. The journal also covers applications of basic ageing research to lifespan extension and disease prevention, offering a comprehensive platform for advancing our understanding of this critical field.