Study Title
Hormetic effect of amyloid-beta peptide in synaptic plasticity and memory
Neurobiology of Aging

Daniela Puzzo, Lucia Privitera, Agostino Palmeri


One of the hot topics in Alzheimer’s disease research field is the “amyloid hypothesis” postulating that the increase and deposition of beta-amyloid peptides (A-beta) is the main pathogenetic factor. However, antiamyloid-based therapies have so far been a failure and, most importantly, growing evidences suggest that A-beta has important physiologic functions. Based on our previous findings demonstrating that low concentrations of A-beta enhanced both synaptic plasticity and memory, whereas high concentrations induced the well-known impairment of cognition, here we show that A-beta acts on hippocampal long-term potentiation and reference memory drawing biphasic dose-response curves. This phenomenon, characterized by low-dose stimulation and high-dose inhibition and represented by a U-shaped or inverted-U-shaped curve, resembles the characteristics of hormesis. The A-beta double role raises important issues on the use of A-beta level reducing agents in Alzheimer’s disease.

December 11, 2011
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