Varghese Merina, Pandey Mritunjay, Samanta Ananda, Gangopadhyay Prasanta Kumar, Mohanakumar Kochupurackal P
Division of Cell Biology and Physiology, Laboratory of Clinical & Experimental Neuroscience, Indian Institute of Chemical Biology (CSIR), Kolkata, West Bengal, India.
J Neurol Sci. 2009 Apr 15;279(1-2):39-42. doi: 10.1016/j.jns.2008.12.021. Epub 2009 Jan 26.
The observation of decline in mitochondrial electron transport chain function, specifically at complex I, in patients with Parkinson's disease (PD) has been reported by several groups. This study investigates whether a defect of mitochondrial function is present in the platelets of PD patients from an Indian population. We found that the NADH dehydrogenase activity in the platelets of PD patients is lower than that in healthy age- and gender-matched controls, while the succinate dehydrogenase activity was similar in both groups. Furthermore, there was no change in either of the activities in patients with Parkinson plus syndrome or atypical parkinsonism. This is the first report indicating a decline in mitochondrial function in the platelets of PD patients from the Indian population, offering further support to the role of a mitochondrial defect in PD.
几个研究小组报告称,观察到帕金森病(PD)患者的线粒体电子传递链功能下降,特别是在复合体I处。本研究调查了印度人群中PD患者的血小板是否存在线粒体功能缺陷。我们发现,PD患者血小板中的NADH脱氢酶活性低于年龄和性别匹配的健康对照者,而两组的琥珀酸脱氢酶活性相似。此外,帕金森叠加综合征或非典型帕金森病患者的这两种活性均无变化。这是第一份表明印度人群中PD患者血小板线粒体功能下降的报告,进一步支持了线粒体缺陷在PD中的作用。