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Mitochondrial ND5 mutations in idiopathic Parkinson's disease.

Author information

Affiliations

  • 1. Department of Neurology, University of Virginia School of Medicine, Charlottesville, VA 22901, USA.
      Authors
    • Parker WD Jr 1
    (1 author)

Biochemical and Biophysical Research Communications, 01 Jan 2005, 326(3):667-669
https://doi.org/10.1016/j.bbrc.2004.11.093 PMID: 15596151 

Abstract 

Idiopathic Parkinson's disease (PD) is characterized by a systemic loss of activity of complex I (NADH:ubiquinone oxidoreductase), the target enzyme of the parkinsonism producing neurotoxin, MPTP. Cybrid experiments strongly suggest that the loss of complex I activity arises from mitochondrial DNA. We prospectively evaluated low frequency, amino acid changing, heteroplasmic mutations in a narrow region of ND5, a mitochondrial gene encoding a complex I subunit, in brain tissue from PD and controls. The presence or absence of amino acid changing mutations correctly classified 15 of 16 samples. Heteroplasmic mutations in a specific region of ND5 largely segregate PD from controls and may be of major pathogenic importance in idiopathic PD.

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Read article at publisher's site: https://doi.org/10.1016/j.bbrc.2004.11.093

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