Somatic mitochondrial DNA mutations in early Parkinson and incidental lewy body disease

Michael T. Lin, Ippolita Cantuti-Castelvetri, Kangni Zheng, Katie E. Jackson, Yong B. Tan, Thomas Arzberger, Andrew J. Lees, Rebecca A. Betensky, M. Flint Beal, David K. Simon

Research output: Contribution to journalArticle

Abstract

Somatic mutations in mitochondrial DNA (mtDNA) are hypothesized to play a role in Parkinson disease (PD), but large increases in mtDNA mutations have not previously been found in PD, potentially because neurons with high mutation levels degenerate and thus are absent in late stage tissue. To address this issue, we studied early stage PD cases and cases of incidental Lewy body disease (ILBD), which is thought to represent presymptomatic PD. We show for the first time that mtDNA mutation levels in substantia nigra neurons are significantly elevated in this group of early PD and ILBD cases.

Original languageEnglish (US)
Pages (from-to)850-854
Number of pages5
JournalAnnals of Neurology
Volume71
Issue number6
DOIs
StatePublished - Jun 2012

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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    Lin, M. T., Cantuti-Castelvetri, I., Zheng, K., Jackson, K. E., Tan, Y. B., Arzberger, T., Lees, A. J., Betensky, R. A., Beal, M. F., & Simon, D. K. (2012). Somatic mitochondrial DNA mutations in early Parkinson and incidental lewy body disease. Annals of Neurology, 71(6), 850-854. https://doi.org/10.1002/ana.23568