进行性核上性麻痹中的额叶功能障碍：氧化应激和线粒体损伤的证据。

Frontal lobe dysfunction in progressive supranuclear palsy: evidence for oxidative stress and mitochondrial impairment.

作者信息

Albers D S, Augood S J, Park L C, Browne S E, Martin D M, Adamson J, Hutton M, Standaert D G, Vonsattel J P, Gibson G E, Beal M F

机构信息

Department of Neurology and Neuroscience, Cornell University Medical College, New York, NY 10021, USA.

出版信息

J Neurochem. 2000 Feb;74(2):878-81. doi: 10.1046/j.1471-4159.2000.740878.x.

DOI:10.1046/j.1471-4159.2000.740878.x

PMID:10646541

Abstract

Recent data from our laboratory have shown a regionally specific increase in lipid peroxidation in postmortem progressive supranuclear palsy (PSP) brain. To extend this finding, we measured activities of mitochondrial enzymes as well as tissue malondialdehyde (MDA) levels in postmortem superior frontal cortex (Brodmann's area 9; SFC) from 14 pathologically confirmed cases of PSP and 13 age-matched control brains. Significant decreases (-39%) in alpha-ketoglutarate dehydrogenase complex/glutamate dehydrogenase ratio and significant increases (+36%) in tissue MDA levels were observed in the SFC in PSP; no differences in complex I or complex IV activities were detected. Together, these results suggest that mitochondrial dysfunction and lipid peroxidation may underlie the frontal metabolic and functional deficits observed in PSP.

摘要

我们实验室最近的数据显示，在死后的进行性核上性麻痹（PSP）大脑中，脂质过氧化存在区域特异性增加。为了扩展这一发现，我们测量了14例经病理证实的PSP病例和13例年龄匹配的对照大脑死后额叶上皮质（布罗德曼9区；SFC）中线粒体酶的活性以及组织丙二醛（MDA）水平。在PSP患者的SFC中观察到α-酮戊二酸脱氢酶复合物/谷氨酸脱氢酶比值显著降低（-39%），组织MDA水平显著升高（+36%）；未检测到复合物I或复合物IV活性的差异。这些结果共同表明，线粒体功能障碍和脂质过氧化可能是PSP中观察到的额叶代谢和功能缺陷的基础。