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臭氧诱导的神经病理学和阿尔茨海默病记忆衰退的观点:临床前证据的系统回顾。

Perspectives of ozone induced neuropathology and memory decline in Alzheimer's disease: A systematic review of preclinical evidences.

机构信息

Department of Pharmacology, SRM College of Pharmacy, SRMIST, SRM Nagar, Kattankulathur, Kancheepuram, 603 203, Tamil Nadu, India.

Department of Pharmacology, SRM College of Pharmacy, SRMIST, SRM Nagar, Kattankulathur, Kancheepuram, 603 203, Tamil Nadu, India.

出版信息

Environ Pollut. 2022 Nov 15;313:120136. doi: 10.1016/j.envpol.2022.120136. Epub 2022 Sep 8.

Abstract

This systematic review aims to discover the plausible mechanism of Ozone in A.D., to boost translational research. The main focus of our review lies in understanding the effects of ozone pollution on the human brain and causing degenerative disease. Owing to the number of works carried out as preclinical evidence in association with oxidative stress and Alzheimer's disease and the lack of systematic review or meta-analysis prompted us to initiate a study on Alzheimer's risk due to ground-level ozone. We found relevant studies from PubMed, ScienceDirect, Proquest, DOAJ, and Scopus, narrowing to animal studies and the English language without any time limit. The searches will be re-run before the final analysis. This work was registered in Prospero with Reg ID CRD42022319360, followed the PRISMA-P framework, and followed the PICO approach involving Population, Intervention/Exposure, Comparison, and Outcomes data. Bibliographic details of 16 included studies were studied for Exposure dose of ozone, duration, exposure, and frequency with control and exposure groups. Primary and secondary outcomes were assessed based on pathology significance, and results were significant in inducing Alzheimer-like pathology by ozone. In conclusion, ozone altered oxidative stress, metabolic pathway, and amyloid plaque accumulation besides endothelial stress response involving mitochondria as the critical factor in ATP degeneration, caspase pathway, and neuronal damage. Thus, ozone is a criteria pollutant to be focused on in mitigating Alzheimer's Disease pathology.

摘要

本系统评价旨在发现臭氧在 AD 中的可能作用机制,以促进转化研究。我们的综述重点在于了解臭氧污染对人脑的影响及其导致退行性疾病的机制。由于已有大量关于氧化应激和阿尔茨海默病的临床前证据,并且缺乏系统评价或荟萃分析,因此我们着手研究由于地面臭氧导致的阿尔茨海默病风险。我们从 PubMed、ScienceDirect、Proquest、DOAJ 和 Scopus 中找到了相关研究,仅限于动物研究且语言为英文,没有时间限制。在最终分析之前,将重新进行搜索。这项工作在 Prospero 中进行了注册,注册号为 CRD42022319360,遵循 PRISMA-P 框架,并采用 PICO 方法,涉及人群、干预/暴露、比较和结局数据。我们研究了 16 项纳入研究的暴露剂量、臭氧暴露的持续时间、频率和对照及暴露组的详细文献。根据病理学意义评估主要和次要结局,结果表明臭氧可诱导类似阿尔茨海默病的病理学变化。总之,臭氧改变了氧化应激、代谢途径和淀粉样斑块积累,此外还涉及内皮细胞应激反应,线粒体作为 ATP 退化、半胱氨酸蛋白酶途径和神经元损伤的关键因素。因此,臭氧是需要重点关注的导致阿尔茨海默病病理学的标准污染物。

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