cAMP, cGMP and Amyloid β: Three Ideal Partners for Memory Formation

Abstract

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.

Keywords: Alzheimer’s disease; amyloid hypothesis; long-term potentiation.