多奈哌齐对阿尔茨海默病患者外周血Aβ1-42和Tau蛋白浓度的影响

Effect of Donepezil on the Concentration of Aβ1-42 and Tau Protein in the Peripheral Blood of Patients with Alzheimer's Disease

中文关键词: 阿尔茨海默病  多奈派齐  Aβ1-42蛋白  Tau蛋白

英文关键词: Alzheimer's disease (AD)  donepezil  β-amyloid peptide 1-42 (Aβ1-42))  Tau protein

中文摘要:

      目的 探讨多奈哌齐对阿尔茨海默病(Alzheimer's disease,AD)患者血浆β淀粉样蛋白(β-amyloid peptide 1-42,Aβ1-42)和Tau蛋白浓度的影响.方法 采用ELISA技术测定48例轻中度AD患者和42例正常对照者血浆Aβ1-42和Tau蛋白浓度,AD组与对照组分别给予多奈哌齐和维生素E口服6个月.结果 AD患者治疗前Aβ1-42蛋白浓度为(41.14 ±6.28) pg/mL,低于对照组(52.87±10.83) pg/mL (P＜ 0.05).多奈哌齐治疗后Aβ1-42蛋白浓度(47.91±7.47) pg/mL,较治疗前升高(P＜0.05).AD患者治疗前Tau蛋白浓度为(22.17±4.93) pg/mL,高于对照组的(18.56±6.21) pg/mL(P＜0.05),治疗后浓度降低到(20.16±4.24) pg/mL,但差异无统计学意义(P＞0.05).结论 多奈哌齐增加AD患者血浆Aβ1-42蛋白浓度,可能通过减少Aβ蛋白的沉积来发挥治疗作用.

英文摘要:

      Objective To discuss the effect of donepezil on the concentration of β-amyloid peptide 1-42 (Aβ1-42)) and Tau protein in patients with Alzheimer's disease (AD).Methods ELISA was applied in detecting the concentration of plasma Aβ1-42 and Tau protein of 48 patients with mild to moderate AD in AD group and 42 norm in control group;oral administration of both donepezil and vitamin E was performed in all the cases in the 2 groups for 6 months.Results Before treatment,the concentration of Aβ1-42 protein of the patients in AD group was (41.14±6.28) pg/mL,lower than that of the cases in control group:(52.87± 10.83) pg/mL (P＜0.05);after the treatment with donepezil,the concentration of Aβ1-42 protein of the patients in AD group increased and was higher than that before treatment (P＜0.05);before treatment,the concentration of Tau protein of the patients in AD group was (22.17±4.93) pg/mL,higher than that in control group:(18.56±6.21) pg/mL (P＜0.05);after treatment,the concentration of Tau protein of the patients in AD group decreased to (20.16 ±4.24) pg/mL,the difference from that before treatment was of no statistical significance (P＞ 0.05).Conclusions Donepezil increases the concentration of Aβ1-42 protein in plasma of AD patients,it may play a therapeutic role by reducing β-amyloid peptide's deposition.