Role of nitric oxide in the aβ25-35 toxicity in vivo

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 hippocampus (Hp) or temporal cortex (TCx), on the nitric oxide (NO) pathways, glial-fibrillary acidic protein (GFAP), 3-nitrotyrosine (3-NT), and the spatial memory of rats one month after the injection. The results showed a significant increase of nitrites in the Hp and TCx of A beta((25-35))-treated rats at the same time that a decrease in the spatial memory and signs of the degeneration process in these areas of the brain occurred. These data suggest that the fraction A beta((25-35)) injected into the Hp or TCx increases NO, which is critical for the neuropathlogical progression and memory impairment in AD.