Emerging evidence indicates that rosiglitazone, a potent agonist of peroxisome proliferator-activated receptor gamma (PPARγ), can prevent or attenuate neurodegeneration in Alzheimers disease (AD), but the mechanisms underlying this effect remain to be fully elucidated.In this study, behavioral testing, electrophysiology methods and live cell imaging technologies were used to investigate the effect of soluble amyloid-β protein (Aβ) oligomers on the synaptic plasticity and synaptic development and to find out wether rosiglitazone can rescue the impairment induced by amyloid-β protein (Aβ) oligomers.We found that administration of Aβ1.42 oligomers through unilateral hippocampal injection significantly attenuated the memory and cognition in rats during morris water maze test.20 μM and 5 μM rosiglitazone improved the memory impairment induced by Aβ1-42 oligomers, while 0.5 μM rosiglitazone has no effect.