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Possible involvement of a mitochondrial translation initiation factor 3 variant causing decreased mRNA levels in Parkinson's disease.

Journal article
Authors Anna Anvret
Caroline Ran
Marie Westerlund
Ann-Christin Thelander
Olof Sydow
Charlotta Lind
Anna Håkansson
Hans Nissbrandt
Dagmar Galter
Andrea Carmine Belin
Published in Parkinson's disease
Volume 2010
Pages 491751
ISSN 2042-0080
Publication year 2010
Published at Institute of Neuroscience and Physiology, Department of Pharmacology
Pages 491751
Language en
Links dx.doi.org/10.4061/2010/491751
Subject categories Medical and Health Sciences

Abstract

Genes important for mitochondrial function have been implicated in Parkinson's disease (PD). Mitochondrial translation initiation factor 3 (MTIF3) is a nuclear encoded protein required for the initiation of complex formation on mitochondrial ribosomes. Dysfunction of MTIF3 may impair mitochondrial function and dopamine neurons appear to be particularly vulnerable to oxidative stress, which may relate to their degeneration in PD. An association was recently reported between the synonymous rs7669(C>T) in MTIF3 and PD in a German case-control material. We investigated rs7669 in a Swedish Parkinson case-control material. The study revealed no significant association of the individual genotypes or alleles with PD. When comparing the combined TT/CT-genotypes versus the CC-genotype, we observed a significant association (P = .0473) with PD. We also demonstrated that the TT-genotype causes a significant decrease in MTIF3 mRNA expression compared to the CC-genotype (P = .0163). Our findings support the hypothesis that MTIF3 may be involved in the etiology of PD.

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