Genetic Screening of the Mitochondrial Rho GTPases MIRO1 and MIRO2 in Parkinson’s Disease

Anna Anvret1, Caroline Ran1, Marie Westerlund1, 2, Olof Sydow3, Thomas Willows3, Lars Olson1, Dagmar Galter1, Andrea Carmine Belin*, 1
1 Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden
2 Present address: Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
3 Department of Neurology, Karolinska University Hospital, Stockholm, Sweden

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© Anvret et al; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden; Tel: +46-8-524 870 51; Fax: +46-8-323 742; E-mail:


MIRO1 and MIRO2 (mitochondrial Ras homolog gene family, member T1 and T2) also referred to as RHOT1 and RHOT2, belong to the mitochondrial Rho GTPase family and are involved in axonal transport of mitochondria in neurons. Because mitochondrial dysfunction is strongly implicated in Parkinson’s disease (PD), MIRO1 and MIRO2 can be considered as new candidate genes for PD. We analyzed two non-synonymous polymorphisms and one synonymous polymorphism in MIRO1 and two non-synonymous polymorphisms in MIRO2, in a Swedish Parkinson case-control material consisting of 241 patients and 307 neurologically healthy controls. None of the analyzed polymorphisms in MIRO1 and MIRO2 were significantly associated with PD. Although we did not find a significant association with PD in our Swedish case-control material, we cannot exclude these Rho GTPases as candidate genes for PD or other neurodegenerative disorders.

Keywords: Association, mitochondria, single nucleotide polymorphism.