Objective:To adopt the brain lesion model of mouse induced by overload aluminum to study the relationship between monoamine oxidase B disorder and neurodegeneration induced by overload aluminum(Al).Method:Aluminum overload models were established by injection of 3μl AlCl3 into lateral ventricle of miceeach day for 5d.The AlCl3 solutions injected in different modelswere with different concentrations and they were 0.125%

0.25%

0.5%.On d10

d20

and d30 after the final administration of AlCl3 solution

the learning and memory function of mice

pathomorphology of hippocampi

and MAO-B activity were determined.Results:Aluminum overload elevated MAO-B activity

caused karyopyknosis and loss of neurons in CA1 area of hippocampi

in dose-and time-dependent manners.Conclusion:The results indicate that neurodegeneration induced by Al toxicity may be related to the monoamine oxidase B homeostasis interfered by Al overload.