Stimulus pattern dependence of the Alzheimer's disease amyloid-β 42 peptide's inhibition of long term potentiation in mouse hippocampal slices

Abstract

Increasing evidence has pointed to inhibition of Long Term Potentiation (LTP) by soluble Aβ42 oligomers as central in the etiology of the learning and memory deficits that are hallmarks of Alzheimer Disease. These effects are thought to occur by an interaction between Aβ42 and certain cellular effectors that induce LTP, however, the precise identity of the Aβ42-interactive signaling molecules is unknown. Identification of such effectors is made more difficult because LTP induced by different stimulation protocols can be expressed through heterogeneous signaling pathways. The aim of this study was to compare differences in the Aβ42-dependent levels of inhibition of LTPs that were induced usin..