Publications by authors named "O I Kechko"

Five bifunctional copper chelating agents, , designed to prevent beta-amyloid (Aβ) aggregation, were synthesized, and the leader compound () was chosen. acts as a bifunctional chelator that can interact with various Aβ aggregates and reduce their neurotoxicity. Reactive oxygen species measurements provided by the Pt-nanoelectrode technique in single Aβ-affected human neuroblastoma SH-SY5Y cells revealed significant antioxidant activity of .

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Article Synopsis
  • - Alzheimer's disease is marked by amyloid-beta peptide (Aβ) forming harmful plaques in the brain, which may worsen the disease.
  • - The amyloid hypothesis suggests that treatments preventing Aβ aggregation or reducing plaques could alter the disease's course; in 2023, the FDA approved lecanemab, a monoclonal antibody targeting Aβ aggregates.
  • - This review explores the role of interactions between zinc ions, a specific Aβ variant (isoD7-Aβ), and a receptor in Aβ aggregation, using various transgenic animal models for research insights.
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Amyloid-β (Aβ) is a peptide formed by 39-43 amino acids, heterogenous by the length of its C-terminus. Aβ constitutes a subnanomolar monomeric component of human biological fluids; however, in sporadic variants of Alzheimer's disease (AD), it forms soluble neurotoxic oligomers and accumulates as insoluble extracellular polymeric aggregates (amyloid plaques) in the brain tissues. The plaque formation is controlled by zinc ions; therefore, abnormal interactions between the ions and Aβ seem to take part in the triggering of sporadic AD.

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virulence factor InlB specifically interacts with the receptors c-Met and gC1q-R. Both receptors are present in non-professional and professional phagocytes, including macrophages. Phylogenetically defined InlB isoforms differently support invasion into non-professional phagocytes.

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Severe acute respiratory syndrome associated coronavirus 2 (SARS-CoV-2) emerged at the end of 2019 and rapidly caused a pandemic that led to the death of >6 million people due to hypercoagulation and cytokine storm. In addition, SARS-CoV-2 triggers a wide array of pathologies, including liver dysfunction and neurological disorders. It remains unclear if these events are due to direct infection of the respective tissues or result from systemic inflammation.

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