Copper and cuproptosis: new therapeutic approaches for Alzheimer's disease

Copper (Cu) plays a crucial role as a trace element in various physiological processes in humans. Nonetheless, free copper ions accumulate in the brain over time, resulting in a range of pathological changes. Compelling evidence indicates that excessive free copper deposition contributes to cognitiv...

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Bibliographic Details
Published in:Frontiers in aging neuroscience 2023-12, Vol.15, p.1300405-1300405
Main Authors: Li, Xiao, Chen, Xinwang, Gao, Xiyan
Format: Article
Language:English
Subjects:
Alzheimer's disease
Antioxidants
Brain
Cell death
Chelating agents
chelators
Cognitive ability
Copper
cuproptosis
Dementia
Disease
Homeostasis
Lipid peroxidation
Lipids
long-term potentiation
Memory
Neurodegenerative diseases
Neuroscience
Oxidative stress
Pathogenesis
Physiology
Proteins
Toxicity
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Summary:Copper (Cu) plays a crucial role as a trace element in various physiological processes in humans. Nonetheless, free copper ions accumulate in the brain over time, resulting in a range of pathological changes. Compelling evidence indicates that excessive free copper deposition contributes to cognitive decline in individuals with Alzheimer's disease (AD). Free copper levels in the serum and brain of AD patients are notably elevated, leading to reduced antioxidant defenses and mitochondrial dysfunction. Moreover, free copper accumulation triggers a specific form of cell death, namely copper-dependent cell death (cuproptosis). This article aimed to review the correlation between copper dysregulation and the pathogenesis of AD, along with the primary pathways regulating copper homoeostasis and copper-induced death in AD. Additionally, the efficacy and safety of natural and synthetic agents, including copper chelators, lipid peroxidation inhibitors, and antioxidants, were examined. These treatments can restore copper equilibrium and prevent copper-induced cell death in AD cases. Another aim of this review was to highlight the significance of copper dysregulation and promote the development of pharmaceutical interventions to address it.
ISSN:1663-4365
1663-4365
DOI:10.3389/fnagi.2023.1300405