Naomi Ruth, Teoh Soo Huat, Embong Hashim, Balan Santhra Segaran, Othman Fezah, Bahari Hasnah, Yazid Muhammad Dain
Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Serdang 43400, Malaysia.
Advanced Medical and Dental Institute, Universiti Sains Malaysia, Kepala Batas 13200, Malaysia.
Antioxidants (Basel). 2023 May 10;12(5):1071. doi: 10.3390/antiox12051071.
Obesity is a chronic low-grade inflammatory condition that induces the generation of oxidative stress and inflammation. This oxidative stress and inflammation stimulate brain atrophy and some morphological changes in the brain that eventually result in cognitive impairments. However, there is no exact study that has summarized the role of oxidative stress and inflammation in obesity and its impact on cognitive impairments. Thus, the objective of this review is to recapitulate the current role of oxidative stress and inflammation in cognitive decline based on in vivo evidence. A comprehensive search was performed in Nature, Medline and Ovid, ScienceDirect, and PubMed, and the search was limited to the past 10 years of publication. From the search, we identified 27 articles to be further reviewed. The outcome of this study indicates that a greater amount of fat stored in individual adipocytes in obesity induces the formation of reactive oxygen species and inflammation. This will lead to the generation of oxidative stress, which may cause morphological changes in the brain, suppress the endogenous antioxidant system, and promote neuroinflammation and, eventually, neuronal apoptosis. This will impair the normal function of the brain and specific regions that are involved in learning, as well as memory. This shows that obesity has a strong positive correlation with cognitive impairments. Hence, this review summarizes the mechanism of oxidative stress and inflammation that induce memory loss based on animal model evidence. In conclusion, this review may serve as an insight into therapeutic development focusing on oxidative stress and inflammatory pathways to manage an obesity-induced cognitive decline in the future.
肥胖是一种慢性低度炎症状态，会引发氧化应激和炎症反应。这种氧化应激和炎症会刺激脑萎缩以及大脑的一些形态学变化，最终导致认知障碍。然而，尚无确切研究总结氧化应激和炎症在肥胖中的作用及其对认知障碍的影响。因此，本综述的目的是根据体内证据概括氧化应激和炎症在认知衰退中的当前作用。我们在《自然》《医学索引》《Ovid》《科学Direct》和《PubMed》中进行了全面检索，检索范围限于过去10年发表的文献。通过检索，我们确定了27篇文章进行进一步综述。本研究结果表明，肥胖个体脂肪细胞中储存的大量脂肪会诱导活性氧的形成和炎症反应。这将导致氧化应激的产生，可能会引起大脑形态学变化、抑制内源性抗氧化系统、促进神经炎症并最终导致神经元凋亡。这会损害大脑以及参与学习和记忆的特定区域的正常功能。这表明肥胖与认知障碍呈强正相关。因此，本综述基于动物模型证据总结了氧化应激和炎症导致记忆丧失的机制。总之，本综述可为未来聚焦于氧化应激和炎症途径以应对肥胖引起的认知衰退的治疗开发提供见解。
