Amyloid-β Enhances Memory

Whether Aβ has a positive function — or is simply an unwanted byproduct created when amyloid precursor protein is cleaved to produce more essential fragments — remains a matter of debate. Evidence from transgenic mice suggests the former: knock-out of enzymes required for Aβ production impairs memory and long-term potentiation (LTP). More evidence for a positive role of Aβ is presented by Puzzo et al.

They found that picomolar (near physiological) amounts of monomeric and oligomeric Aβ42 enhanced LTP in mouse hippocampal slices and strengthened reference and contextual fear memory in vivo.

In contrast, nanomolar concentrations reduced LTP. The enhancement of LTP appeared to occur presynaptically, likely by increasing calcium accumulation, and it required activation of α7 nicotinic acetylcholine receptors.

Whether monomeric Aβ, oligomeric Aβ, or both was responsible for the enhancement is unknown.