Literature DB >> 8293280

Electron transfer complexes I and IV of platelets are abnormal in Parkinson's disease but normal in Parkinson-plus syndromes.

R Benecke1, P Strümper, H Weiss.   

Abstract

Using a technique which requires only 100 ml blood we investigated the electron transfer complexes (ETC) I, III and IV in platelet mitochondria of 44 control subjects, 27 patients with idiopathic Parkinson's disease and eight patients with Parkinson-plus syndromes due to multiple system atrophy. In both control subjects and patients, ETC measurements were repeated at intervals of several months. The activities varied considerably among normal subjects, but intra-individual variation of ETC activities were low at repetitive measurements. In normal subjects there was no correlation between enzyme activities and age or training state. There was no difference in enzyme activities between smokers and non-smokers in the control group. Complex I activity was lower in Parkinson's disease patients than in controls (14 versus 29 nmol/min/mg platelet protein; P < 0.001). Furthermore, the group difference in complex IV activity also reached statistical significance (83 versus 58 nmol/min/mg platelet protein; P < 0.001). Additionally, in some Parkinson's disease patients, activities of complex III were low and lay outside the control range, but the group difference did not reach significance. There was no correlation between complex I activity and disease duration or severity as well as the daily L-dopa dose in Parkinson's disease patients. Repeated measurements in five Parkinson's disease patients in the earliest stages of their illness demonstrated that the decrease in complex I and IV activities can develop rapidly within 1 year. In Parkinson-plus patients suffering from multiple system atrophy the ETC activities were normal.

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Year:  1993        PMID: 8293280     DOI: 10.1093/brain/116.6.1451

Source DB:  PubMed          Journal:  Brain        ISSN: 0006-8950            Impact factor:   13.501


  52 in total

1.  Mutations in mitochondrial complex III uniquely affect complex I in Caenorhabditis elegans.

Authors:  Wichit Suthammarak; Phil G Morgan; Margaret M Sedensky
Journal:  J Biol Chem       Date:  2010-10-22       Impact factor: 5.157

2.  Characterization of basal ganglia dysfunction in Leber 'plus' disease.

Authors:  C O Hanemann; H Hefter; G Schlaug; R J Seitz; H J Freund; R Benecke
Journal:  J Neurol       Date:  1996-03       Impact factor: 4.849

Review 3.  The unresolved role of mitochondrial DNA in Parkinson's disease: An overview of published studies, their limitations, and future prospects.

Authors:  Amica C Müller-Nedebock; Rebecca R Brennan; Marianne Venter; Ilse S Pienaar; Francois H van der Westhuizen; Joanna L Elson; Owen A Ross; Soraya Bardien
Journal:  Neurochem Int       Date:  2019-06-21       Impact factor: 3.921

4.  Complex I deficiency in Parkinson's disease frontal cortex.

Authors:  W Davis Parker; Janice K Parks; Russell H Swerdlow
Journal:  Brain Res       Date:  2007-11-01       Impact factor: 3.252

Review 5.  Mitochondrial dysfunction in the limelight of Parkinson's disease pathogenesis.

Authors:  Rebecca Banerjee; Anatoly A Starkov; M Flint Beal; Bobby Thomas
Journal:  Biochim Biophys Acta       Date:  2008-11-14

Review 6.  Neuroproteomics as a promising tool in Parkinson's disease research.

Authors:  Ilse S Pienaar; William M U Daniels; Jürgen Götz
Journal:  J Neural Transm (Vienna)       Date:  2008-06-04       Impact factor: 3.575

Review 7.  Mitochondrial approaches for neuroprotection.

Authors:  Rajnish K Chaturvedi; M Flint Beal
Journal:  Ann N Y Acad Sci       Date:  2008-12       Impact factor: 5.691

8.  Complex I function is defective in complex IV-deficient Caenorhabditis elegans.

Authors:  Wichit Suthammarak; Yu-Ying Yang; Phil G Morgan; Margaret M Sedensky
Journal:  J Biol Chem       Date:  2008-12-12       Impact factor: 5.157

Review 9.  Current perspective of mitochondrial biology in Parkinson's disease.

Authors:  Navneet Ammal Kaidery; Bobby Thomas
Journal:  Neurochem Int       Date:  2018-03-14       Impact factor: 3.921

10.  Platelet-mediated transformation of mtDNA-less human cells: analysis of phenotypic variability among clones from normal individuals--and complementation behavior of the tRNALys mutation causing myoclonic epilepsy and ragged red fibers.

Authors:  A Chomyn; S T Lai; R Shakeley; N Bresolin; G Scarlato; G Attardi
Journal:  Am J Hum Genet       Date:  1994-06       Impact factor: 11.025

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