Cerebral Hypoperfusion In Pathogenesis Of AD In Rats

Objiective: To estimate the etiology of brain ischemia in Alzheimer's disease in rats.Methods: Male Wistar rats weighing 300-350g were used for this study. Ischemia was produced by permanently ligating the left internal carotid artery. Sham-operated controls were treated similarly to the ischemic group. But the left internal carotid artery was not occluded. Iron concentration and consecutive changes (at 4,8,16,32 weeks after operation) in peripheral blood were tested by kit. SOD, MDA and NO concentrations and consecutive changes (at 4, 8, 16, 32 weeks after operation) in peripheral blood and brain tissue were tested by kits. Immunocytochemical staining was used to show immune plaques of ?-amyloid protein (A?) in brain tissues. Results: Iron concentrations in blood at 4, 8 weeks in the operated groups were significantly higher than in the control groups (P<0.05). Iron concentrations in blood at 16, 32 weeks were not higher than in the control groups (P>0.05). MDA and NO concentrations at 4 weeks after operation in peripheral blood and brain tissue markedly increased as comparing with control groups (P<0.05). MDA and NO concentrations at 8,16,32 weeks after operation in peripheral blood and brain tissue were not higher than in the control groups (P>0.05). SOD activity at 4weeks after operation in peripheral blood and brain tissue markedly decreased as comparing with that of control groups (P<0.05). There were no significantly increase of SOD activity at 8,16,32 weeks after operation in peripheral blood and brain tissue as comparing with that of the control groups(P>0.05). A? immune plaques in the left brain tissues were been shown until 32 weeks after ischemia. There were not A? immune plaques found in the right brain tissues.Conclusion: Cerebral ischemia can induce an increase iron concentration in blood, free radical damage, and A? immune plaques. Our research support the hypothesis that longer cerebral ischemia may play an important role in AD, and iron malmetabolism, free radical may be contributed to AD.