Journal
ANNALS OF NEUROLOGY
Volume 71, Issue 6, Pages 850-854Publisher
WILEY-BLACKWELL
DOI: 10.1002/ana.23568
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Funding
- NIH National Institute of Neurological Disorders and Stroke [K02NS043311, R03NS053840, R01NS058988]
- Harvard University
- NIH National Institute on Aging [R01AG20729]
- United States Army Medical Research and Materiel Command [W81XWH-04-1-0802]
- American Federation for Aging Research-Paul Beeson Physician Faculty Scholarship
- Massachusetts General Hospital/Massachusetts Institute of Technology Morris Udall Center of Excellence in PD Research [NIH NS38372]
- American Parkinson's Disease Association Advanced Center for Parkinson Research at Massachusetts General Hospital
- Harvard Neurodiscovery Center
- Harvard Catalyst
- German Federal Ministry of Research and Technology
- Public Health Service [R24MH068855, P50AG005134]
- NIH [UL1 RR025758]
- Harvard University and its affiliated academic health care centers
- Columbia University
- Harvard Medical School
- MJFF
- European Commission
- PSP Association
- Weston Trust-Reta Lila Howard Foundation
- Novartis
- Teva
- Meda
- Boehringer Ingelheim
- GSK
- Ipsen
- Lundbeck
- Allergan
- Orion
- BIAL
- Noscira
- Roche
- NIH (NINDS)
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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. Ann Neurol 2012;71:850854
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