Analysis of the Effect of Neuroprotectors That Reduce the Level of Degeneration of Neurons in the Rat Hippocampus Caused by Administration of Beta-Amyloid Peptide Aβ25-35.

Deposition of beta-amyloid peptide in the brain observed in Alzheimer's disease contributes to the development of cognitive deficits. We studied the abilities of different neuroprotectors to prevent or reduce degeneration of hippocampal neurons in rat brain 14 and 45 days after single intrahippocampal injection of beta-amyloid peptide 25-35 (Aβ25-35). Cytological analysis of the neurons of the hippocampal CA1 and CA3 fields showed predominant damage to CA1 neurons in 14 days and CA3 neurons in 45 days after Aβ25-35 administration. Single preliminary administrations of neuroprotectors fullerene C60FWS (antioxidant), neuromedin (nonselective inhibitor of acetylcholinesterase), and AM404 (activator of the endocannabinoid system) largely prevented neurodegeneration of neurons. Fullerene produced the most pronounced protective effect, which can be explained by its ability to prevent aggregation of proteins and destroy Aβ25-35 fibrils. The combined use of these neuroprotectors can provide the basis for the development of new approaches to prevention and treatment of Alzheimer's disease.