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

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

Abstract read

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Article in Bulletin of experimental biology and medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

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5 · Who and what money

Authors and funding

5 authors.

M A GrudenFederal Research Center for Innovator and Emerging Biomedical and Pharmaceutical Technologies, Moscow, Russia. gruden_ma@academpharm.ru.

T V DavydovaInstitute of General Pathology and Pathophysiology, Moscow, Russia.

A M RatmirovFederal Research Center for Innovator and Emerging Biomedical and Pharmaceutical Technologies, Moscow, Russia.

L A VetrileInstitute of General Pathology and Pathophysiology, Moscow, Russia.

Z I StorozhevaFederal Research Center for Innovator and Emerging Biomedical and Pharmaceutical Technologies, Moscow, Russia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

AgingAmyloidAntibodiesBasic Helix-Loop-Helix ProteinsCalgranulin BGlutamic AcidMemory DisordersSpatial MemoryAnimalsGene Expression RegulationHippocampusMaleMaze LearningMiceMice, Inbred C57BLPrefrontal CortexAmyloidAntibodiesAscl1 protein, mouseBasic Helix-Loop-Helix ProteinsCalgranulin BGlutamic AcidS100A9 protein, mouseantibodies to glutamateASCL1 genememorymiceS100A9 protein fibrils

Identifiers

PMID40866648

DOI10.1016/j.apsb.2023.10.007

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.