The Role of Copper in Alzheimer's Disease Etiopathogenesis: An Updated Systematic Review.

IF 3.9 3区环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES

Toxics Pub Date : 2024-10-17 DOI:10.3390/toxics12100755

Angela Sabalic, Veronica Mei, Giuliana Solinas, Roberto Madeddu

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引用次数: 0

Abstract

Background: Alzheimer's disease (AD) is the most common cause of dementia and cognitive decline in the elderly. Although the etiology of AD is unknow, an increase in amyloid precursor protein (APP) leads to the toxic aggregation of Aβ plaques. Several factors, such as hypertension, diabetes, dyslipidemia, smoking, hormonal changes, and metal exposure, could increase the risk of developing AD. In this review, we will examine the role of copper (Cu) in the pathophysiology of AD, as well as the mechanisms involved in neurotoxicity and cognitive decline.

Methods: This review was conducted in accordance with PRISMA guidelines. We performed a comprehensive literature analysis over the last ten years on AD and Cu. Only late-onset Alzheimer's disease was considered; only studies on elderly people of both sexes were included.

Results: A total of seven articles were picked for this review, three studies focused on non-ceruloplasmin-bound Copper (non-Cp-Cu) and four on ceruloplasmin-bound Copper (Cp-Cu). The results showed higher Cu concentrations in patients compared to healthy controls.

Conclusions: Elevated concentrations of Cu may contribute to the progression of AD, potentially interacting with ATP7B mutations, oxidative stress (OS), and amyloid-β plaques. Future research is needed to provide more robust evidence and better characterize the relationship between AD and Cu.

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铜在阿尔茨海默病发病机制中的作用：最新系统综述。

背景：阿尔茨海默病（AD）是导致老年人痴呆和认知能力下降的最常见原因。虽然阿尔茨海默病的病因尚不清楚，但淀粉样前体蛋白（APP）的增加会导致 Aβ 斑块的毒性聚集。高血压、糖尿病、血脂异常、吸烟、荷尔蒙变化和金属接触等多种因素都可能增加罹患AD的风险。在这篇综述中，我们将研究铜（Cu）在AD病理生理学中的作用，以及参与神经毒性和认知能力下降的机制：本综述根据 PRISMA 指南进行。我们对过去十年间有关 AD 和铜的文献进行了全面分析。只考虑了晚发性阿尔茨海默病；只纳入了对男女老年人的研究：本综述共选取了七篇文章，其中三篇研究的重点是非髓磷蛋白结合铜（non-Cp-Cu），四篇研究的重点是髓磷蛋白结合铜（Cp-Cu）。结果显示，与健康对照组相比，患者体内的铜浓度更高：结论：铜浓度升高可能会与ATP7B突变、氧化应激（OS）和淀粉样蛋白-β斑块相互作用，导致AD进展。未来的研究需要提供更有力的证据，并更好地描述AD与铜之间的关系。

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

Toxics Chemical Engineering-Chemical Health and Safety

CiteScore

4.50

自引率

10.90%

发文量

681

审稿时长

6 weeks

期刊介绍： The Journal accepts papers describing work that furthers our understanding of the exposure, effects, and risks of chemicals and materials in humans and the natural environment as well as approaches to assess and/or manage the toxicological and ecotoxicological risks of chemicals and materials. The journal covers a wide range of toxic substances, including metals, pesticides, pharmaceuticals, biocides, nanomaterials, and polymers such as micro- and mesoplastics. Toxics accepts papers covering: The occurrence, transport, and fate of chemicals and materials in different systems (e.g., food, air, water, soil); Exposure of humans and the environment to toxic chemicals and materials as well as modelling and experimental approaches for characterizing the exposure in, e.g., water, air, soil, food, and consumer products; Uptake, metabolism, and effects of chemicals and materials in a wide range of systems including in-vitro toxicological assays, aquatic and terrestrial organisms and ecosystems, model mammalian systems, and humans; Approaches to assess the risks of chemicals and materials to humans and the environment; Methodologies to eliminate or reduce the exposure of humans and the environment to toxic chemicals and materials.