Department of Neurology, Iwate Medical University, Morioka, Japan.
Dement Geriatr Cogn Disord. 2009;28(5):449-54. doi: 10.1159/000256209. Epub 2009 Nov 10.
BACKGROUND/AIM: The contribution of mitochondrial dysfunction and oxidative stress to the pathogenesis of Alzheimer's disease (AD) has previously been described. We aimed to investigate whether the balance between the oxidized and reduced forms of coenzyme Q-10 (CoQ-10) is related to the pathogenesis of AD.
Thirty patients with AD (69.0 +/- 4.1 years) and 30 healthy control subjects (63.8 +/- 16.4 years) were enrolled in this study. Concentrations of oxidized CoQ-10 and reduced CoQ-10 were measured by high-performance liquid chromatography using an electrochemical detector.
The percentage of oxidized/total CoQ-10 in the cerebrospinal fluid (%CoQ-10, CSF) was significantly higher in the untreated AD group (78.2 +/- 18.8%) than in the control group (41.3 +/- 10.4%, p < 0.001), and there was a significant negative correlation between %CoQ-10 and the duration of the illness (r(s) = -0.93, p < 0.001).
These findings in living AD patients suggest a possible role for %CoQ-10 in the pathogenesis of the early stage of AD development.
背景/目的：先前已有研究描述了线粒体功能障碍和氧化应激对阿尔茨海默病（AD）发病机制的贡献。我们旨在研究辅酶 Q-10（CoQ-10）氧化和还原形式之间的平衡是否与 AD 的发病机制有关。
本研究纳入了 30 名 AD 患者（69.0 +/- 4.1 岁）和 30 名健康对照者（63.8 +/- 16.4 岁）。采用高效液相色谱电化学检测法测定脑脊液中氧化型 CoQ-10 和还原型 CoQ-10 的浓度。
未经治疗的 AD 组脑脊液中氧化型/总 CoQ-10 的百分比（%CoQ-10，CSF）明显高于对照组（78.2 +/- 18.8%比 41.3 +/- 10.4%，p < 0.001），且%CoQ-10 与病程呈显著负相关（r(s) = -0.93，p < 0.001）。
这些在活 AD 患者中的发现提示%CoQ-10 可能在 AD 早期发展的发病机制中发挥作用。
