Objective To investigate the effect of electroacupuncture(EA) of "Baihui"(GV20) and "Yongquan"(KI1) on the expression of amyloid β protein(Aβ) and low density lipoprotein(LDL) receptor-related protein 1(LRP1) in the hippo-campal sulcus microvessels in amyloid precursor protein(APP) 695V717Ⅰ transgenic mice

so as to study its mechanism underlying relief of Alzheimer Disease(AD).Methods Twelve APP 695V717Ⅰ transgenic mice were randomly divided into model group and EA group.Six C 57 BL/6 mice were used as the control group.EA(2Hz/100Hz

3-5mA) was applied to "Baihui"(GV20) and "Yongquan"(KI1) for 15min

once every other day for three months.The learning-memory ability of mice was detected by using Lashley Ⅲ water maze system.The expression level of Aβ1-42

and LRP1 in the hippocampal sulcus microvessels were measured by immunohistochemistry.Results Water maze test showed that the swimming duration from the start to the goal box(terminal) in the Lashley Ⅲ water maze was significantly longer in the model group than in the control group(P<0.05)

suggesting a markedly lower learning-memory capacity of APP 695V717Ⅰ transgenic mice.Compared with the model group

the swimming duration in the EA group was decreased considerably(P<0.05).The integrated optical density(IOD) value of hippo-campal Aβ1-42 immunoreaction(IR) positive products in the model group was significantly higher than that in the control group(P<0.01) and the IOD value of hippocampal LRP 1 IR-positive products in the model group was apparently lo-wer than that in the control group(P<0.01).In comparison with the model group

the IOD value of Aβ 1-42 IR-positive products in the EA group was obviously lower than that in the model group(P<0.05)

while that of LRP1 IR-positive products in the EA group was significantly higher than that in the model group(P<0.05)

suggesting down-regulation of hippocampal Aβ1-42 expression and up-regulation of LRP1 expression after EA

and reduction of deposition of Aβ in the cerebral microvessels after EA.Conclusion EA can improve the learning-memory capacity of APP transgenic mice

which is closely related to its effects in up-regulating hippocampal LRP1 expression and down-regulating hippocampal Aβ1-42 expression.