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Dopamine transporter SPECT in patients with mitochondrial disorders
  1. M Minnerop1,
  2. C Kornblum1,
  3. A Y Joe2,
  4. K Tatsch4,
  5. W S Kunz3,
  6. T Klockgether1,
  7. U Wüllner1,
  8. M J Reinhardt2
  1. 1Department of Neurology, University of Bonn, Bonn, Germany
  2. 2Department of Nuclear Medicine, University of Bonn
  3. 3Department of Epileptology, University of Bonn
  4. 4Department of Nuclear Medicine, University of Munich, Munich, Germany
  1. Correspondence to:
 Dr Ullrich Wüllner
 Department of Neurology, University of Bonn, Sigmund-Freud-Strasse 25, Bonn 53105, Germany; wuellneruni-bonn.de

Abstract

Background: Mitochondrial disorders may affect basal ganglia function. In addition, decreased activity of complex I of the mitochondrial electron transport chain has been linked to the pathogenesis of dopaminergic cell loss in Parkinson’s disease.

Objective :To investigate the dopaminergic system in patients with known mitochondrial disorders and complex I deficiency.

Methods: Dopamine transporter density was studied in 10 female patients with mitochondrial complex I deficiency by 123I-FP-CIT (N-β-fluoropropyl-2β-carbomethyl-3β-(4-iodophenyl)-nortropane) SPECT.

Results: No differences in 123I-FP-CIT striatal binding ratios were observed and no correlation of the degree of complex I deficiency and striatal binding ratios could be detected.

Conclusions: These data argue against the possibility that mitochondrial complex I deficiency by itself is sufficient to elicit dopaminergic cell loss.

  • CPEO, chronic progressive external ophthalmoplegia
  • DAT, dopamine transporter
  • SPECT, single photon emission computed tomography
  • dopamine
  • 123 I-FP-CIT SPECT
  • mitochondrial disorders

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Footnotes

  • Competing interests: KT has been paid by Amersham Health for speaking and organising educational seminars. He also has a consultancy contract and has been reimbursed for attending conferences organised by the company. The department receives research funds from the company.