Amyloid-B Enhances Memory

Amyloid-B  (AB)  Is generally considered a toxic agent in Alzheimer’s disease, but it is also released during synaptic transmission in healthy brains.  Whether AB  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 AB  Production impairs memory and long-term potentiation (LTP).  More evidence for a positive role of AB  Is presented by Puzzo et al.  They found that picomolar (near physiological) amounts of monomeric and oligomeric AB42 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 a7 nicotinic acetylcholine receptors.  Whether monomeric AB, oligomeric AB, or both was responsible for the enhancement is unknown.

Tagged as: , Alzheimer's disease, amyloid-b, long term potentiation, LTP, synaptic transmission