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Abstract <p><b>Objective:</b> The aim of this study was to evaluate the cytotoxic effect of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and β-amyloid (Aβ1-42) co-aggregates on human mesenchymal cells reprogrammed into a neuronal phenotype. <b>Methods:</b> Co-aggregates were formed by incubating recombinant GAPDH and synthetic Aβ1-42 in the presence of tissue transglutaminase, which provides covalent cross-linking of proteins. <b>Results:</b> The data obtained demonstrate that GAPDH–Aβ1-42 co-aggregates have pronounced neurotoxicity, but are able to activate protective and compensatory mechanisms, including the chaperone apparatus. <b>Conclusions:</b> The results emphasize the need to develop therapeutic strategies aimed at blocking the GAPDH–Aβ1-42 interaction and supporting cellular protective pathways to prevent neurodegeneration</p>

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The Role of the Glyceraldehyde-3-phosphate Dehydrogenase and β-Amyloid Complex in the Activation of the Cellular Chaperone System

  • 期刊论文

  • 发表日期：

    2025年9月30日

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  • E. A. Dutysheva,
  • A. V. Yurakova,
  • A. A. Sakharov,
  • I. V. Guzhova,
  • B. A. Margulis,
  • V. F. Lazarev

摘要

Abstract

Objective: The aim of this study was to evaluate the cytotoxic effect of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and β-amyloid (Aβ1-42) co-aggregates on human mesenchymal cells reprogrammed into a neuronal phenotype. Methods: Co-aggregates were formed by incubating recombinant GAPDH and synthetic Aβ1-42 in the presence of tissue transglutaminase, which provides covalent cross-linking of proteins. Results: The data obtained demonstrate that GAPDH–Aβ1-42 co-aggregates have pronounced neurotoxicity, but are able to activate protective and compensatory mechanisms, including the chaperone apparatus. Conclusions: The results emphasize the need to develop therapeutic strategies aimed at blocking the GAPDH–Aβ1-42 interaction and supporting cellular protective pathways to prevent neurodegeneration