Beta-amyloid (Aβ) peptide accumulation has long been implicated in the pathogenesis of Alzheimer's disease (AD). Hippocampal network hyperexcitability in the early stages of the disease leads to increased epileptiform activity and eventually cognitive decline. We found that acute application of 250 nM soluble Aβ42 oligomers increased Ca activity in hippocampal neurons in parallel with a significant decrease in activity in Aβ42-treated interneurons.
View Article and Find Full Text PDF