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Abstract <p>β-Amyloid peptides (Aβ), which play a crucial role in the pathogenesis of Alzheimer’s disease by forming toxic oligomeric species, are known to affect mitochondrial function. In this study, luciferin-luciferase assay was used to assess changes in ATP production by mitochondria isolated from human neuroblastoma SH-SY5Y cells cultured in the presence of monomeric Aβ at a nanomolar concentration. ATP synthesis rates were measured in the presence of substrates specific for respiratory chain complexes&#xa0;I,&#xa0;II, and&#xa0;IV alongside inhibitors targeting the other complexes. Aβ significantly reduced both the rate of ATP generation and amount of ATP synthesized by mitochondria. This effect of Aβ on ATP synthesis did not result from a direct influence on the respiratory chain complexes&#xa0;I,&#xa0;II, and&#xa0;IV. Our findings provide insights into possible causes of mitochondrial dysfunction in neurons in Alzheimer’s disease.</p>

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Beta-Amyloid Suppresses Mitochondrial ATP Production in Human Neuroblastoma Cells

  • 期刊论文

  • 发表日期：

    2026年2月1日

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  • Yuliya A. Zagryadskaya,
  • Semen V. Nesterov,
  • Vladimir A. Mitkevich,
  • Sergey A. Kozin,
  • Anastasia K. Kryuchkova,
  • Galina Yu. Lomakina,
  • Mikhail S. Karbyshev,
  • Eduard V. Bocharov,
  • Alexander A. Makarov,
  • Ivan S. Okhrimenko

摘要

Abstract

β-Amyloid peptides (Aβ), which play a crucial role in the pathogenesis of Alzheimer’s disease by forming toxic oligomeric species, are known to affect mitochondrial function. In this study, luciferin-luciferase assay was used to assess changes in ATP production by mitochondria isolated from human neuroblastoma SH-SY5Y cells cultured in the presence of monomeric Aβ at a nanomolar concentration. ATP synthesis rates were measured in the presence of substrates specific for respiratory chain complexes I, II, and IV alongside inhibitors targeting the other complexes. Aβ significantly reduced both the rate of ATP generation and amount of ATP synthesized by mitochondria. This effect of Aβ on ATP synthesis did not result from a direct influence on the respiratory chain complexes I, II, and IV. Our findings provide insights into possible causes of mitochondrial dysfunction in neurons in Alzheimer’s disease.