Amyloid-β25-35 impairs memory and increases NO in the temporal cortex of rats

beta-Amyloid plays an important role in the neurodegeneration process of Alzheimer's disease (AD), but its neurotoxic mechanisms are not clear. It has been associated with the increase of oxidative stress and cognitive impairment because the beta-amyloid peptide 25-35 (A beta((25-35))) has the critical neurotoxic properties of the full-length A beta(1-42). Our present study shows the role of A beta((25-35)) when injected into the temporal cortex on the nitric oxide pathways, 3-nitrotyrosine, neuronal death, and the spatial memory of rats I month after the injection. Our data showed that A beta((25-35)) increases oxidative stress, causes neuronal damage, and decreases spatial memory in rats. Notably, the injection of the fraction A beta((25-35)) caused an increase of nNOS and iNOS immunoreactivity in the temporal cortex and hippocampus. We demonstrated a significant increase of reactive astrocytosis, which was accompanied by neuronal damage in the temporal cortex and hippocampus of rats injected with A beta((25-35)). These data suggest that the fraction A beta((25-35)) injected into the temporal cortex might contribute to understanding the role of nitric oxide on the biological changes related to the neuropathological progression and the memory impairment in AD. (C) 2008 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.