Serum paraoxonase activity changes in patients with Alzheimer's disease and vascular dementia
Serum paraoxonase activity changes in patients with Alzheimer's disease and vascular dementia
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DOI：
10.1007/s004060200013
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发表时间：
2002-04-01
影响因子：
4.7
通讯作者：
Degrell, I
中科院分区：
文献类型：
--
作者：
Paragh, G;Balla, P;Degrell, I
阿尔茨海默病（AD）和血管性痴呆（VAD）的患病率随着人口老龄化而增加。脂蛋白在AD发病机制中的作用尚不清楚：apoE（2）提供保护，apoE（3）是中性的，而apoE（4）促进疾病的发展。HDL相关对氧磷酶是一种可减少LDL氧化的抗氧化酶。本研究采用全自动血脂分析仪测定了30例AD、40例VAD患者和40例健康对照者的血脂指标及血清对氧磷酶活性。使用对氧磷作为底物，通过电化学计量法测量对氧磷酶活性。对氧磷酶的表型分布用双底物法测定，以对氧磷和苯乙酸为底物，我们的结果发现，大多数AD患者具有apoE（4）亚型，与其他研究一致。在VAD和AD患者中，我们发现与对照组相比，总胆固醇显著升高（C：4.71 +/- 0.89，VAD：6.3 +/- 0.8，AD：6.52 +/- 0.7 mmol/l; p < 0.01）和LDL-胆固醇水平（C：2.6 +/- 0.6，VAD：3.96 +/- 0.8，AD：3.84 +/- 0.6 mmol/l; p < 0.001）。高密度脂蛋白相关的抗氧化剂，对氧磷酶活性在患者组中没有显著差异，但与健康对照受试者相比，对氧磷酶活性在两个患者组中均显著降低（C：188 ± 55 U/l; AD：131 ± 37，VAD：151 ± 50 l;我们的研究结果表明，HDL相关的抗氧化能力的缺陷在阿尔茨海默病和血管性痴呆的发病机制中起作用。
The prevalence of Alzheimer's disease (AD) and vascular dementia (VAD) increases with aging of the population. The role of lipoproteins in the pathogenesis of AD is unclear: apoE(2) offers protection and apoE(3) is neutral, while apoE(4) promotes the development of the disease.Recently, several studies have confirmed the role of oxidative stress in the pathogenesis of AD and VAD. HDL-associated paraoxonase is one of the antioxidative enzymes that may reduce LDL oxidation. In our study, we investigated the lipid parameters of the sera and the serum paraoxonase activity in patients with AD and VAD.Lipid parameters were determined by an autoanalyzer in 30 AD patients, 40 VAD patients and 40 healthy, age-matched control (C) subjects. Paraoxonase activity was measured spectrophotometrically using paraoxon as the substrate. The phenotypic distribution of paraoxonase was determined by the dual substrate method, using paraoxon and phenylacetate as substrates.In our results, we found that most of the patients with AD had the apoE(4) isoform, consistent with other studies. In the VAD and AD patients we found significantly higher total-cholesterol compared to the control group (C: 4.71 +/- 0.89, VAD: 6.3 +/- 0.8, AD: 6.52 +/- 0.7 mmol/l; p < 0.01) and LDL-cholesterol levels (C: 2.6 +/- 0.6, VAD: 3.96 +/- 0.8, AD: 3.84 +/- 0.6 mmol/l; p < 0.001). The HDL-associated antioxidant, paraoxonase activity did not differ significantly in the patient groups, but compared to the healthy control subjects, paraoxonase activity was significantly lower in both of the patient groups (C: 188 +/- 55 U/l; AD: 131 +/- 37, VAD: 151 +/- 50 l; p < 0.05).Our results suggest that the defect in HDL-associated antioxidant capacity plays a role in the pathogenesis of Alzheimer's disease and vascular dementia.