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<p>Immunological correction of cognitive processes impaired due to the action of neurotoxic amyloidogenic forms of proinflammatory protein S100A9, a promoter of the inflammatory-amyloid cascade occurring in Alzheimer’s disease, is poorly understood. Chronic intranasal administration of S100A9 fibrils leads to suppression of spatial memory formation in the Morris water maze in 12-month-old C57BL/6J mice and to an increase in activity of the <i>ASCL1</i> gene involved in neurogenesis at the stage of cell differentiation, in the hippocampus and prefrontal cortex. In the case of combined administration of S100A9 fibrillar structures and antibodies to glutamate, the duration of the latency of reaching the platform in the water maze as well as <i>ASCL1</i> gene expression in the hippocampus and prefrontal cortex returned to normal, but not in the cerebellum where a decrease in <i>ASCL1</i> gene activity was observed.</p>

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Effect of Glutamate Antibodies on ASCL1 Gene Expression in Aging Mice with Spatial Memory Impairment Caused by Amyloid Fibrils of the Proinflammatory Protein S100A9

  • 期刊论文

  • 发表日期：

    2025年6月1日

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  • M. A. Gruden,
  • T. V. Davydova,
  • A. M. Ratmirov,
  • L. A. Vetrile,
  • Z. I. Storozheva

摘要

Immunological correction of cognitive processes impaired due to the action of neurotoxic amyloidogenic forms of proinflammatory protein S100A9, a promoter of the inflammatory-amyloid cascade occurring in Alzheimer’s disease, is poorly understood. Chronic intranasal administration of S100A9 fibrils leads to suppression of spatial memory formation in the Morris water maze in 12-month-old C57BL/6J mice and to an increase in activity of the ASCL1 gene involved in neurogenesis at the stage of cell differentiation, in the hippocampus and prefrontal cortex. In the case of combined administration of S100A9 fibrillar structures and antibodies to glutamate, the duration of the latency of reaching the platform in the water maze as well as ASCL1 gene expression in the hippocampus and prefrontal cortex returned to normal, but not in the cerebellum where a decrease in ASCL1 gene activity was observed.