Post-stroke cognitive impairment: exploring molecular mechanisms and omics biomarkers for early identification and intervention

IF 3.5 3区医学 Q2 NEUROSCIENCES

Frontiers in Molecular Neuroscience Pub Date : 2024-05-23 DOI:10.3389/fnmol.2024.1375973

Qiuyi Lu, Anqi Yu, Juncai Pu, Dawei Chen, Yujie Zhong, Dingqun Bai, Lining Yang

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引用次数: 0

Abstract

Post-stroke cognitive impairment (PSCI) is a major stroke consequence that has a severe impact on patients’ quality of life and survival rate. For this reason, it is especially crucial to identify and intervene early in high-risk groups during the acute phase of stroke. Currently, there are no reliable and efficient techniques for the early diagnosis, appropriate evaluation, or prognostication of PSCI. Instead, plenty of biomarkers in stroke patients have progressively been linked to cognitive impairment in recent years. High-throughput omics techniques that generate large amounts of data and process it to a high quality have been used to screen and identify biomarkers of PSCI in order to investigate the molecular mechanisms of the disease. These techniques include metabolomics, which explores dynamic changes in the organism, gut microbiomics, which studies host–microbe interactions, genomics, which elucidates deeper disease mechanisms, transcriptomics and proteomics, which describe gene expression and regulation. We looked through electronic databases like PubMed, the Cochrane Library, Embase, Web of Science, and common databases for each omics to find biomarkers that might be connected to the pathophysiology of PSCI. As all, we found 34 studies: 14 in the field of metabolomics, 5 in the field of gut microbiomics, 5 in the field of genomics, 4 in the field of transcriptomics, and 7 in the field of proteomics. We discovered that neuroinflammation, oxidative stress, and atherosclerosis may be the primary causes of PSCI development, and that metabolomics may play a role in the molecular mechanisms of PSCI. In this study, we summarized the existing issues across omics technologies and discuss the latest discoveries of PSCI biomarkers in the context of omics, with the goal of investigating the molecular causes of post-stroke cognitive impairment. We also discuss the potential therapeutic utility of omics platforms for PSCI mechanisms, diagnosis, and intervention in order to promote the area’s advancement towards precision PSCI treatment.

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脑卒中后认知障碍：探索分子机制和 omics 生物标志物，以进行早期识别和干预

脑卒中后认知障碍（PSCI）是脑卒中的主要后果，严重影响患者的生活质量和存活率。因此，在脑卒中急性期对高危人群进行早期识别和干预尤为重要。目前，还没有可靠、高效的技术来对 PSCI 进行早期诊断、适当评估或预后判断。相反，近年来脑卒中患者的大量生物标志物已逐渐与认知障碍联系起来。能生成大量数据并进行高质量处理的高通量组学技术已被用于筛选和鉴定 PSCI 的生物标志物，以研究该疾病的分子机制。这些技术包括探索生物体动态变化的代谢组学、研究宿主与微生物相互作用的肠道微生物组学、阐明更深层疾病机制的基因组学、描述基因表达和调控的转录组学和蛋白质组学。我们查阅了 PubMed、Cochrane 图书馆、Embase、Web of Science 等电子数据库以及每种 omics 的常用数据库，以寻找可能与 PSCI 病理生理学相关的生物标志物。我们总共找到了 34 项研究：其中代谢组学研究 14 项，肠道微生物组学研究 5 项，基因组学研究 5 项，转录组学研究 4 项，蛋白质组学研究 7 项。我们发现神经炎症、氧化应激和动脉粥样硬化可能是 PSCI 发病的主要原因，而代谢组学可能在 PSCI 的分子机制中发挥作用。在本研究中，我们总结了各omics技术的现有问题，并讨论了omics背景下PSCI生物标志物的最新发现，目的是研究卒中后认知障碍的分子原因。我们还讨论了全息技术平台在脑卒中后认知障碍的机制、诊断和干预方面的潜在治疗作用，以促进该领域向脑卒中后认知障碍的精准治疗迈进。

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

Frontiers in Molecular Neuroscience NEUROSCIENCES-

CiteScore

5.70

自引率

2.10%

发文量

669

审稿时长

14 weeks

期刊介绍： Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.

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