cAMP and cGMP are well established second messengers required for long-term potentiation (LTP) and memory formation/consolidation. By contrast, amyloid β (Aβ), mostly known as one of the main culprits for Alzheimer's disease (AD), has received relatively little attention in the context of plasticity and memory. Of note, however, low physiological concentrations of Aβ seem necessary for LTP induction and for memory formation. This should come as no surprise, since hormesis emerged as a central dogma in biology. Additionally, recent evidence indicates that Aβ is one of the downstream effectors for cAMP and cGMP to trigger synaptic plasticity and memory. We argue that these emerging findings depict a new scenario that should change the general view on the amyloidogenic pathway, and that could have significant implications for the understanding of AD and its pharmacological treatment in the future.

中文翻译：

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cAMP、cGMP 和淀粉样蛋白 β：记忆形成的三个理想伙伴

cAMP 和 cGMP 是长期增强 (LTP) 和记忆形成/巩固所需的公认第二信使。相比之下，淀粉样蛋白 β (Aβ)，主要被称为阿尔茨海默病 (AD) 的罪魁祸首之一，在可塑性和记忆方面受到的关注相对较少。然而，值得注意的是，低生理浓度的 Aβ 似乎是 LTP 诱导和记忆形成所必需的。这应该不足为奇，因为兴奋剂作为生物学的中心法则出现。此外，最近的证据表明 Aβ 是 cAMP 和 cGMP 触发突触可塑性和记忆的下游效应物之一。我们认为，这些新发现描绘了一种新情况，应该会改变对淀粉样蛋白通路的普遍看法，