To investigate improvement of melatonm on leammg and memory impairment induced by amyloid β- peptide 25-35 (Aβ25-35) in elder rats. METHODS: Step-down type passive avoidance test, shuttle-box test, and Morris water maze were used together to determine effects of Aβ25-35 and melatonin on learning and memory. Pathological changes were observed by HE, Congo red, and Ag staining. RESULTS: The elder rats were injected bilaterally Aβ25-35 20 g into the hippocampus to induce learning and memory dysfunction. Melatonin administration (0.1, 1, and 10mg/kg, ig×8 d) to the Aβ25-35-treated rats prolonged the latency, shortened the total stimulating time, and decreased the number of errors in the step-down test. Suttle-box test showed that melatonin improved amnesic rats" performace at the same doses. Melatonin (0.1, 1, and 10mg/kg), giving for 10 d, could enhance the spatial resolution of amnesic rats in Morris water maze test. Also in Aβ25-35-treated group, a decrease in the number of neurons in cortex and hippocampus, a massive glial reaction, and neurophilic phenomenon were detected by HE staining; the positive vascular amyloidosis by Congo red and fibrils by Ag staining were observed. Melatonin (0.1 and 1 mg/kg)could inhibit above pathological changes in Aβ25-35-group. CONCLUSION: Melatonin improved the impaired learning and memory induced by Aβ25-35 in elder rats.

This work investigated the ability of melatonin to prevent oxidative damage in brain tissue induced by injection of beta-amyloid peptide 25-35 (Ab25-35) in middle-aged rats. The Morris water maze was used to evaluate the cognitive function of the rats. Thiobarbituric acid-reactive substances and antioxidative enzymes (superoxide dismutase and glutathione peroxidase) activities were measured. It was found that injection of (Ab25-35) (20

To investigate whether melatonin protects neurons from apoptosis, we used amyloid beta-peptide 25±35 (Ab25-35) to induce apoptosis in cultured hippocampal neurons, and monitored the apoptotic activity of the neurons with or without melatonin treatment. Present study shows that melatonin at concentrations of 1×10－6 and 1×10－5mol/L prevents neuronal morphological changes induced by apoptosis, as characterized by the shrunken and rounded morphology caused by condensed chromatin and fragmented DNA. Melatonin further exhibited the ability to inhibit apoptotic internucleosomal DNA degradation. Moreover, ow cytometric analysis of cell cycle demonstrated that melatonin abolished the Ab25-35-induced apoptotic peak. Our results suggest that melatonin may play an important role to protect neurons from Ab25±35-induced apoptosis.