艾地苯醌对帕金森患者额叶磁共振波谱成像的影响
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摘要
目的:利用磁共振波谱成像研究艾地苯醌对帕金森患者额叶神经细胞代谢的影响,从神经生化角度探讨艾地苯醌对帕金森病(PD)的潜在治疗作用及可能作用机制。方法:2017年10月—2018年6月我院收治的PD患者66例为研究对象,按随机数字表法分为对照组与研究组,各33例。对照组采取常规药物治疗,研究组在对照组基础上加用艾地苯醌(30 mg,tid),治疗一疗程后以帕金森综合评分量表(UPDRS-Ⅲ)评估两组治疗效果,以氢质子磁共振波谱(1H-MRS)检查两组患者额叶神经细胞代谢的变化情况。结果:两组治疗后额叶N-乙酰天门氡氨酸(NAA)/肌酸(Cr)、胆碱复合物(Cho)/Cr值较治疗前显著升高,且研究组高于对照组,差异有统计学意义(P <0.01);治疗后两组UPDRS-Ⅲ评分较治疗前明显改善,且研究组优于对照组,差异有统计学意义(P <0.05)。结论:艾地苯醌口服可提高PD患者的治疗效果,提高额叶NAA/Cr及Cho/Cr值,可为帕金森病的诊治提供新的思路。
Objective: The effect of idebenone on the metabolism of frontal lobe neurocytes in patients with Parkinson's disease was studied by magnetic resonance spectroscopy imaging. The potential therapeutic effect of idebenone on Parkinson's disease(PD) and its possible mechanism were investigated from the perspective of neurobiochemistry. Methods: 66 patients with PD admitted to our hospital from October 2017 to June 2018 were selected as subjects investigated and randomly divided into a control group and a study group, 33 cases each. The patients in the control group were given conventional drug therapy, and the patients in the study group were treated with idebenone(30 mg, tid) on the basis of the control group. After one course of treatment, the therapeutic effect in the two groups was evaluated by Parkinson's Comprehensive Rating Scale(UPDRS-Ⅲ), and the changes in the metabolism of frontal lobe neurocytes of the patients in the two groups were examined by hydrogen proton magnetic resonance spectroscopy(1 H-MRS). Results: The value of N-acetyl-aspartate(NAA)/creatine(Cr) and the value of choline complex(Cho)/Cr in the frontal lobes of the two groups after treatment were significantly higher than those before treatment, and the values in the study group were higher than those in the control group, with statistically significant differences(P<0.01). The UPDRS-Ⅲ scores in the two groups after treatment were significantly improved compared with those before treatment, and the scores in the study group were better than those in the control group, with statistically significant difference(P<0.05). Conclusion: Oral administration of idebenone can improve its therapeutic effect on PD patients and increase the values of NAA/Cr and Cho/Cr in frontal lobes, which can provide a new idea for the diagnosis and treatment of Parkinson's disease.
Objective: The effect of idebenone on the metabolism of frontal lobe neurocytes in patients with Parkinson's disease was studied by magnetic resonance spectroscopy imaging. The potential therapeutic effect of idebenone on Parkinson's disease(PD) and its possible mechanism were investigated from the perspective of neurobiochemistry. Methods: 66 patients with PD admitted to our hospital from October 2017 to June 2018 were selected as subjects investigated and randomly divided into a control group and a study group, 33 cases each. The patients in the control group were given conventional drug therapy, and the patients in the study group were treated with idebenone(30 mg, tid) on the basis of the control group. After one course of treatment, the therapeutic effect in the two groups was evaluated by Parkinson's Comprehensive Rating Scale(UPDRS-Ⅲ), and the changes in the metabolism of frontal lobe neurocytes of the patients in the two groups were examined by hydrogen proton magnetic resonance spectroscopy(1 H-MRS). Results: The value of N-acetyl-aspartate(NAA)/creatine(Cr) and the value of choline complex(Cho)/Cr in the frontal lobes of the two groups after treatment were significantly higher than those before treatment, and the values in the study group were higher than those in the control group, with statistically significant differences(P<0.01). The UPDRS-Ⅲ scores in the two groups after treatment were significantly improved compared with those before treatment, and the scores in the study group were better than those in the control group, with statistically significant difference(P<0.05). Conclusion: Oral administration of idebenone can improve its therapeutic effect on PD patients and increase the values of NAA/Cr and Cho/Cr in frontal lobes, which can provide a new idea for the diagnosis and treatment of Parkinson's disease.
引文
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[13]Imada I,Fujita T,Sugiyama Y,et al.Effects of idebenone and related compounds on respiratory activities of brain mitochondria,and on lipid peroxidation of their membranes[J].Arch Gerontol Geriatr,1989,8(3):323-341.
[14]Benarroch EE.N-acetylaspartate and N-acetylaspartylglu tamate:neurobiology and clinical significance[J].Neurolo gy,2008,70(16):1353-1357.
[15]Camicioli RM,Hanstock CC,Bouchard TP,et al.Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson’s disease[J].Mov Disord,2007,22(3):382-386.
[16]Sulzer D,Cassidy C,Horga G,et al.Neuromelanin detection by magnetic resonance imaging(MRI)and its promise as a biomarker for Parkinson’s disease[J].NPJ Parkinsons Dis,2018,4:11.
[17]de Celis AB,Hidalgo-Tobón SS,Menéndez-González M,et al.Magnetic Resonance Techniques Applied to the Diagnosis and Treatment of Parkinson’s Disease[J].Front Neurol,2015,6:146.
[2]Macdonald R,Barnes K,Hastings C,et al.Mitochondrial abnormalities in Parkinson’s disease and Alzheimer’s disease:can mitochondria be targeted therapeutically[J].Biochem Soc Trans,2018,46(4):891-909.
[3]Zhu ZG,Sun MX,Zhang WL,et al.The efficacy and safety of coenzyme Q10 in Parkinson’s disease:a meta-analysis of randomized controlled trials[J].Neurol Sci,2017,38(2):215-224.
[4]Bola?os JP,Moro MA,Lizasoain I,et al.Mitochondria and reactive oxygen and nitrogen species in neurological disorders and stroke:Therapeutic implications[J].Adv Drug Deliv Rev,2009,61(14):1299-1315.
[5]Wu G,Shen YJ,Huang MH,et al.Proton MR Spectroscopy for Monitoring Pathologic Changes in the Substantia Nigra and Globus Pallidus in Parkinson Disease[J].AJR Am JRoentgenol,2016,206(2):385-389.
[6]中华医学会神经病学分会帕金森病及运动障碍学组,中国医师协会神经内科医师分会帕金森病及运动障碍专业.中国帕金森病的诊断标准(2016版)[J].中华神经科杂志,2016,49(4):268-271.
[7]Leibson CL,Long KH,Maraganore DM,et al.Direct medical costs associated with Parkinson’s disease:a populationbased study[J].Mov Disord,2006,21(11):1864-1871.
[8]Shults CW,Haas R.Clinical trials of coenzyme Q10 in neurological disorders[J].Biofactors,2005,25(1-4):117-126.
[9]Bose A1,Beal MF.Mitochondrial dysfunction in Parkinson’s disease[J].J Neurochem,2016,139(S1):216-231.
[10]Mischley LK,Allen J,Bradley R.Coenzyme Q10 deficiency in patients with Parkinson’s disease[J].J Neurol Sci,2012,318(1-2):72-75.
[11]Shults CW,Oakes D,Kieburtz K,et al.Effects of coenzyme q10 in early Parkinson disease:evidence of slowing of the functional decline[J].Arch Neurol,2002,59(10):1541-1550.
[12]Abdel Baky NA,Zaidi ZF,Fatani AJ,et al.Nitric oxide pros and cons:The role of L-arginine,a nitric oxide precursor,and idebenone,a coenzyme-Q analogue in ameliorating cerebral hypoxia in rat[J].Brain Res Bull,2010,83(1-2):49-56.
[13]Imada I,Fujita T,Sugiyama Y,et al.Effects of idebenone and related compounds on respiratory activities of brain mitochondria,and on lipid peroxidation of their membranes[J].Arch Gerontol Geriatr,1989,8(3):323-341.
[14]Benarroch EE.N-acetylaspartate and N-acetylaspartylglu tamate:neurobiology and clinical significance[J].Neurolo gy,2008,70(16):1353-1357.
[15]Camicioli RM,Hanstock CC,Bouchard TP,et al.Magnetic resonance spectroscopic evidence for presupplementary motor area neuronal dysfunction in Parkinson’s disease[J].Mov Disord,2007,22(3):382-386.
[16]Sulzer D,Cassidy C,Horga G,et al.Neuromelanin detection by magnetic resonance imaging(MRI)and its promise as a biomarker for Parkinson’s disease[J].NPJ Parkinsons Dis,2018,4:11.
[17]de Celis AB,Hidalgo-Tobón SS,Menéndez-González M,et al.Magnetic Resonance Techniques Applied to the Diagnosis and Treatment of Parkinson’s Disease[J].Front Neurol,2015,6:146.