In recent years, a significant progress was made in understanding molecular mechanisms of long-term memory. Long-term memory formation requires strengthening of neuronal connections (LTP, long-term potentiation) associated with structural rearrangement of neurons. The key role in the synthesis of proteins essential for these rearrangements belong to mTOR (mammalian target of rapamycin) complexes and signaling pathways involved in mTOR regulation. Suppression of mTOR activity may impair synaptic plasticity and long-term memory, while mTOR activation inhibits autophagy, thereby potentiating amyloidosis and development of Alzheimer's disease (AD) accompanied by irreversible memory loss. Because of this, suppression/inhibition of mTOR might have unpredictable consequences on memory. The Nrf2/ARE signaling pathway affects almost all mitochondrial processes. The activation of this pathway improves memory and exhibits therapeutic effect in AD. In this review, we discuss the crosstalk between the Nrf2/ARE signaling and mTOR in the maintenance of synaptic plasticity. Nrf2 pathway can be activated by pharmacological agents and by changes in mitochondria functioning accompanying various neuronal dysfunctions.

中文翻译：

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mTOR和Nrf2 / ARE信号通路之间的串扰是改善长期增强作用的目标。

近年来，在理解长期记忆的分子机制方面取得了重大进展。长期记忆形成需要加强与神经元结构重排有关的神经元连接（LTP，长期增强）。这些重排所必需的蛋白质合成中的关键作用是mTOR（雷帕霉素的哺乳动物靶标）复合物和参与mTOR调控的信号通路。抑制mTOR活性可能会损害突触可塑性和长期记忆，而mTOR激活会抑制自噬，从而增强淀粉样变性和阿尔茨海默氏病（AD）的发展，并伴有不可逆的记忆丧失。因此，抑制/抑制mTOR可能会对记忆产生不可预测的后果。Nrf2 / ARE信号传导途径影响几乎所有的线粒体过程。该途径的激活改善了记忆并在AD中表现出治疗作用。在这篇综述中，我们讨论了Nrf2 / ARE信号传导与mTOR在维持突触可塑性之间的串扰。Nrf2途径可以通过药理剂激活，并通过伴随各种神经元功能障碍的线粒体功能变化来激活。