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目的探讨叶酸缺乏对APP/PS1双转基因阿尔茨海默病（Alzheimer’s disease, AD）模型小鼠脑组织中早老素1(Presenilin1)基因表达和β-淀粉样蛋白(amyloid-β, Aβ)沉积的影响。方法将6月龄APP/PS1双转基因AD模型小鼠24只，随机分为AD叶酸缺乏组(AD+FA-D)和AD叶酸对照组(AD+FA-N)，每组12只，12只正常同月龄C57小鼠作为阴性对照组（WT+FA-N）。AD+FA-D组给予叶酸缺乏饲料，AD+FA-N组和WT+FA-N组给予正常饲料。免疫组织化学技术检测脑组织β-淀粉样蛋白沉积；实时定量 PCR(RT-PCR)和荧光原位杂交（FISH）检测脑组织中 PS1 mRNA表达；免疫印迹（Western blot）和免疫组织化学法检测脑组织中PS1蛋白表达。结果 WT+FA-N组脑组织Aβ沉积低于AD+FA-N组(P<0.05)；AD+FA-D组高于AD+FA-N组(P<0.05)；WT+FA-N组PS1 mRNA和蛋白表达均低于AD+FA-N组(P<0.05)；AD+FA-D组均高于AD+FA-N组(P<0.05)。结论叶酸缺乏可以增加APP/PS1双转基因AD模型小鼠脑组织中PS1 mRNA和蛋白表达并促进β-淀粉样蛋白沉积。[营养学报，2015，37（1）：27－31]“,”Objective To explore the effects of folic acid deficiency on brain Presenilin 1 (PS1) gene expression and amyloid-βdeposition in APP/PS1 transgenic mice, a model for Alzheimer’s disease (AD). Methods Twenty four 6-month-old APP/PS1 transgenic mice were randomly divided into AD folic acid deficiency group (AD+FA-D) (n=12) and AD folic acid normal group (AD+FA-N) (n=12). Twelve 6-month-old C57 normal mice were set as the wild type normal group (WT+FA-N). AD+FA-D mice were fed the folic acid deficiency diet and AD+FA-N and WT+FA-N mice fed the normal diet. Brain amyloid-β deposition was measured by immunohistochemistry. The expression of brain PS1 mRNA was measured by real time PCR and in situ fluorescence hybridization. The expression of brain PS1 protein was detected by Western blot. Results In mouse brain, amyloid-β deposition in WT+FA-N group was lower than in AD+FA-N group (P<0.05). Amyloid-βdeposition in AD+FA-D group was higher than in AD+FA-N group (P<0.05). PS1 mRNA and protein expression in WT+FA-N group were lower than in AD+FA-N group (P<0.05). PS1 mRNA and protein expression in AD+FA-D group was higher than in AD+FA-N group (P<0.05). Conclusion Folic acid deficiency increased the expression of brain PS1 mRNA and protein and promoted amyloid-βdeposition in APP/PS1 transgenic mice.