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氧化应激和炎症在血管性痴呆发病机制及治疗中的作用

The Role of Oxidative Stress and Inflammation in the Pathogenesis and Treatment of Vascular Dementia.

作者信息

Altahrawi Aseel Y, James Antonisamy William, Shah Zahoor A

机构信息

Department of Pharmacology and Experimental Therapeutics, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, Toledo, OH 43614, USA.

Department of Medicinal and Biological Chemistry, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, Toledo, OH 43614, USA.

出版信息

Cells. 2025 Apr 17;14(8):609. doi: 10.3390/cells14080609.

DOI:10.3390/cells14080609
PMID:40277934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12026122/
Abstract

Vascular dementia (VaD) is a heterogeneous group of brain disorders caused by cerebrovascular pathologies and the second most common cause of dementia, accounting for over 20% of cases and posing an important global health concern. VaD can be caused by cerebral infarction or injury in critical brain regions, including the speech area of the dominant hemisphere or arcuate fasciculus of the dominant hemisphere, leading to notable cognitive impairment. Although the exact causes of dementia remain multifactorial and complex, oxidative stress (reactive oxygen species), neuroinflammation (TNFα, IL-6, and IL-1β), and inflammasomes are considered central mechanisms in its pathology. These conditions contribute to neuronal damage, synaptic dysfunction, and cognitive decline. Thus, antioxidants and anti-inflammatory agents have emerged as potential therapeutic targets in dementia. Recent studies emphasize that cerebrovascular disease plays a dual role: first, as a primary cause of cognitive impairment and then as a contributor to the manifestation of dementia driven by other factors, such as Alzheimer's disease and other neurodegenerative conditions. This comprehensive review of VaD focuses on molecular mechanisms and their consequences. We provided up-to-date knowledge about epidemiology, pathophysiological mechanisms, and current therapeutic approaches for VaD.

摘要

血管性痴呆(VaD)是由脑血管病变引起的一组异质性脑部疾病,是痴呆的第二大常见病因,占病例的20%以上,是一个重要的全球健康问题。VaD可由关键脑区的脑梗死或损伤引起,包括优势半球的语言区或优势半球的弓状束,导致明显的认知障碍。尽管痴呆的确切病因仍然是多因素且复杂的,但氧化应激(活性氧)、神经炎症(TNFα、IL-6和IL-1β)和炎性小体被认为是其病理过程中的核心机制。这些情况会导致神经元损伤、突触功能障碍和认知能力下降。因此,抗氧化剂和抗炎药物已成为痴呆潜在的治疗靶点。最近的研究强调,脑血管疾病具有双重作用:首先,作为认知障碍的主要原因,其次,作为由其他因素(如阿尔茨海默病和其他神经退行性疾病)驱动的痴呆表现的促成因素。这篇对VaD的全面综述聚焦于分子机制及其后果。我们提供了有关VaD的流行病学、病理生理机制和当前治疗方法的最新知识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b97/12026122/87b166d93ba5/cells-14-00609-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b97/12026122/f7c13ab42e25/cells-14-00609-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b97/12026122/87b166d93ba5/cells-14-00609-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b97/12026122/f7c13ab42e25/cells-14-00609-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b97/12026122/87b166d93ba5/cells-14-00609-g002.jpg

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