Soluble beta-amyloid[25-35] reversibly impairs hippocampal synaptic plasticity and spatial learning

Abstract Beta-amyloid is a peptide that appears to be responsible for cognitive impairments in patients with Alzheimer's disease. Recent research shows that soluble oligomers of beta-amyloid affect synaptic activity and learning, well before any amyloid has aggregated into plaques. Here we show that injection of 3 × 10 nmol amyloid [25–35] i.c.v. transiently impairs learning of a radial arm maze and the induction of hippocampal long-term potentiation. Furthermore, hippocampal field potentials had been recorded over a period of 21 days and were found to be reduced from day 9 to day 15 ( P P P