| Background Gradual cognitive decline during normal aging is a common phenomenon observed in humans and animals. The most widely highlighted cognitive change associated with aging is learning and memory. A portion of old humans are ultimately afflicted with Alzheimer's disease (AD).Thus, it is extremely valuable to study the mechanisms of age-related decline in learning and memory for understanding the development and pathogenesis of AD. Rodent animals are excellent models to reach the goal. In decades, many aging researchers focused on the mouse models. Increasing body of evidence indicated: it has been reported that the level of synaptotagmin (Syt), a presynaptic protein, decreases in the brains of patients with AD. On the other hand, it is remains to be debated whether the Syt level changes with normal aging. It is well known that (3-amyloid peptide (A(3) plays critical roles in AD pathogenesis. It has been reported that sumoylation, covalent modification of cellular proteins by small ubiquitin-like modifier (SUMO) proteins, regulates Aβ generation. Increased protein sumoylation resulting from overexpression of SUMO-3 dramatically reduces Aβ production. So far, it has not been reported for the expression pattern of SUMO-3 during aging.Objective ①To study the effects of age on relative levels of synaptotagmin I in frontol lobe in SAMP8 and C57BL/6 mice, and in dorsal hippocampus, ventral hippocampus and olfactory bulb in C57BL/6 mice; ② To explore the effects of age on relative levels of SUMO-3 in the dorsal hippocampus, ventral hippocampus and olfactory bulb in C57BL/6 mice. |