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<p>Copper (Cu) is a vital trace element essential for numerous neurological functions, such as neurotransmission and antioxidant defense mechanisms. Nevertheless, Cu dyshomeostasis has been increasingly associated with neurodegenerative diseases, particularly Alzheimer’s disease (AD).</p><p>This review provides an overview of the intricate mechanisms of Cu homeostasis in the brain, detailing the pathways through which Cu enters neural tissues and its subsequent metabolic roles. We also discuss the emerging concept of cuproptosis, a Cu-dependent regulated cell death mechanism, and highlight its relevance to AD pathophysiology. Furthermore, we examine the interplay between glutamate, a key excitatory neurotransmitter, and cuproptosis, illustrating how alterations in glutamate levels may exacerbate Cu toxicity and contribute to neuronal degeneration in AD. Additionally, we review several compounds with the potential to modulate Cu concentrations, emphasizing their therapeutic implications for restoring Cu balance and mitigating neurodegenerative processes.</p><p>By integrating current findings on Cu metabolism, cuproptosis, and glutamate interactions, this review provides novel insights into potential therapeutic interventions that may help prevent or slow AD progression.</p>

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The interactions of copper, glutamate, and cuproptosis: insights into brain health and Alzheimer’s disease pathology

  • 期刊论文

  • 发表日期：

    2025年12月1日

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  • Maryam Alsadat Mousavi,
  • Shakiba Salarvandian,
  • Sara Rafiee,
  • Mahya Mohammadi,
  • Fariba Khodagholi,
  • Pegah Javadpour

摘要

Copper (Cu) is a vital trace element essential for numerous neurological functions, such as neurotransmission and antioxidant defense mechanisms. Nevertheless, Cu dyshomeostasis has been increasingly associated with neurodegenerative diseases, particularly Alzheimer’s disease (AD).

This review provides an overview of the intricate mechanisms of Cu homeostasis in the brain, detailing the pathways through which Cu enters neural tissues and its subsequent metabolic roles. We also discuss the emerging concept of cuproptosis, a Cu-dependent regulated cell death mechanism, and highlight its relevance to AD pathophysiology. Furthermore, we examine the interplay between glutamate, a key excitatory neurotransmitter, and cuproptosis, illustrating how alterations in glutamate levels may exacerbate Cu toxicity and contribute to neuronal degeneration in AD. Additionally, we review several compounds with the potential to modulate Cu concentrations, emphasizing their therapeutic implications for restoring Cu balance and mitigating neurodegenerative processes.

By integrating current findings on Cu metabolism, cuproptosis, and glutamate interactions, this review provides novel insights into potential therapeutic interventions that may help prevent or slow AD progression.