BRIEF RESEARCH REPORT article

Front. Cell. Neurosci.

Sec. Cellular Neurophysiology

Volume 19 - 2025 | doi: 10.3389/fncel.2025.1629492

This article is part of the Research TopicMemory processing in health and disease: linking behavioral, circuits, and molecular scales.View all articles

Memory Reconsolidation Impairment by Amyloid beta (1-42) and Its Prevention by Non-competitive Antagonists of NMDA Receptors

Provisionally accepted
  • Lomonosov Moscow State University, Moscow, Russia

The final, formatted version of the article will be published soon.

In a healthy brain, the reactivation of memories under conditions of novelty leads to their labilization and subsequent reconsolidation. However, if plasticity of the nervous system is reduced reconsolidation mechanisms may be disrupted, leading to weakening and loss of existing memory. We hypothesize that such self-degradation of old memory due to its reactivation in the compromised brain may lead to progressive memory loss in Alzheimer's disease. Preventing memory lability when accessing it, may slow down such engram degradation. To test these hypotheses, we first examined whether beta-amyloid peptide Aβ1-42 can impair reconsolidation of memory in one-trial passive avoidance task in young chicks. Next, we examined the possibility to prevent such reminder-associated amnesia by administering a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 prior to memory reactivation. Finally, we compared the memory protecting effects of two noncompetitive NMDA antagonists, MK-801 and memantine which is a clinically used medication for treatment of Alzheimer's disease. We found that administration of Aβ1-42 prior to memory reactivation in passive avoidance task in chicks impaired its subsequent reconsolidation. Concurrent systemic injection of MK-801 or memantine prevented this impairment. Our data thus support the hypothesis about the possible role of impaired reconsolidation in the progressive deterioration of old memories in neurodegenerative diseases, particularly in Alzheimer's disease. This hypothesis offers a new explanation for the protective effects of memantine and suggests the possibility of similar effects with other NMDA receptor antagonists.

Keywords: Memory, reconsolidation, chicks, β-Amyloid, NMDA antagonists, Memantine

Received: 15 May 2025; Accepted: 09 Jul 2025.

Copyright: © 2025 Tiunova, Diffine and Anokhin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Konstantin Anokhin, Lomonosov Moscow State University, Moscow, Russia

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.