Normal platelet mitochondrial complex I activity in Huntington's disease

被引：21

作者：

Powers, William J.

Haas, Richard H.

Le, Thuy

Videen, Tom O.

Hershey, Tamara

McGee-Minnich, Lori

Perlmutter, Joel S.

机构：

[1] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA

[2] Washington Univ, Sch Med, Mallinckrodt Inst Radiol, St Louis, MO USA

[3] Washington Univ, Sch Med, Dept Neurosurg, St Louis, MO USA

[4] Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA

[5] Univ Calif San Diego, Dept Pediat, San Diego, CA 92103 USA

[6] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA

[7] Washington Univ, Sch Med, Dept Anat & Neurobiol, St Louis, MO 63110 USA

[8] Washington Univ, Sch Med, Program Phys Therapy, St Louis, MO USA

来源：

NEUROBIOLOGY OF DISEASE | 2007年 / 27卷 / 01期

关键词：

Huntington's disease; mitochondria; electron transport system; platelets; human;

D O I：

10.1016/j.nbd.2007.04.008

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Two small case series of platelet mitochondrial complex I activity assays in Huntington's Disease (HD) report discrepant results. We measured platelet complex I and complex I/III activity in 21 subjects with early gene-positive HD and 14 age-matched controls. The 21 participants with HD that we studied are greater than the total of 16 in the two previously published of platelet ETS activity in HD. Reductions > 10% were excluded with 80% confidence. A systemic defect in complex I activity is not present in early HD when striatal neuronal degeneration is already present. (c) 2007 Elsevier Inc. All rights reserved.

引用

页码：99 / 101

页数：3

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