Journal
JOURNAL OF NEUROSCIENCE
Volume 35, Issue 18, Pages 7304-7311Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0190-15.2015
Keywords
age-related macular degeneration; mitochondria; mitochondrial DNA; oxidative damage; retina; retinal pigment epithelium
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Funding
- Arnold and Mabel Beckman Initiative for Macular Research
- Foundation Fighting Blindness
- University of Minnesota Academic Health Center Grant for Faculty Development
- Minnesota Lions Vision Foundation
- National Institutes of Health [T32-AG029796]
- University of Minnesota Diversity of Views and Experiences
- Research to Prevent Blindness
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Age-related macular degeneration (AMD) is the leading cause of blindness among older adults in the developed world. Although the pathological mechanisms have not been definitively elucidated, evidence suggests a key role for mitochondrial (mt) dysfunction. The current study used our unique collection of human retinal samples graded for the donor's stage of AMD to address fundamental questions about mtDNA damage in the retina. To evaluate the distribution of mtDNA damage in the diseased retina, damage in the retinal pigment epithelium (RPE) and neural retina from individual donors were compared. To directly test a long-held belief that the macula is selectively damaged with AMD, RPE mtDNA damage was measured in the macula and peripheral sections from individual donors. Small segments of the entire mt genome were examined to determine whether specific regions are preferentially damaged. Our results show that mtDNA damage is limited to the RPE, equivalent mtDNA damage is found in the macular and peripheral RPE, and sites of damage are localized to regions of the mt genome that may impact mt function. These results provide a scientific basis for targeting the RPE mitochondria with therapies that protect and enhance mt function as a strategy for combating AMD.
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