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为探讨铝和早老性痴呆（ＡＤ）及其他神经退行性疾病之间的关系及其作用机理，使用原子吸收，免疫组化和Ｎｏｒｔｈｅｒｎ印迹法等检测方法，观察饮用含铝饮水６个月的大鼠脑皮层中Ａｌ３＋和淀粉样β－蛋白前体（β－ＡＰＰ６９５）ｍＲＮＡ及皮层和海马区胶质原酸性纤维蛋白（ＧＦＡＰ）的含量变化．结果发现，ＡｌＣｌ３（７．４和１４．８ｍｍｏｌ·Ｌ－１）在引起脑皮层中铝的含量明显增高的同时，皮层和海马ＧＦＡＰ免疫组化阳性指数升高，皮层β－ＡＰＰ６９５ｍＲＮＡ的含量增加．在饮水铝浓度为１４．８ｍｍｏｌ·Ｌ－１时，β－ＡＰＰ６９５ｍＲＮＡ的相对含量是对照组的２．５倍．结果表明，长期铝接触可以引起胶质细胞增生和β－ＡＰＰ表达的改变．提示铝可能是ＡＤ等神经退行性疾患的一个致病或促发因素．
To explore the relationship between aluminum and Alzheimer’s disease (AD) and other neurodegenerative diseases and its mechanism of action, we used atomic absorption, immunohistochemistry and Northern blot to detect the effect of drinking aluminum-containing drinking water for 6 months Changes of Al3 + and β-APP695 mRNA in rat cerebral cortex and content of glial fibrillary acidic protein (GFAP) in cortex and hippocampus. The results showed that AlCl3 (7.4 and 14.8mmol·L-1) increased the content of aluminum in cerebral cortex while the positive index of GFAP immunohistochemistry in cortex and hippocampus increased and the content of β-APP695mRNA in cortex increased. The relative content of β-APP695mRNA was 2.5 times that of the control group when drinking aluminum concentration was 14.8mmol·L-1. The results show that long-term aluminum exposure can cause changes in glial cell proliferation and β-APP expression. Tip aluminum may be AD and other neurodegenerative diseases, a pathogenic or pro-inflammatory factors.