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Neurobiol Aging. 2015 Oct;36(10):2869-76. doi: 10.1016/j.neurobiolaging.2015.06.010. Epub 2015 Jun 15.

Mitochondrial decline precedes phenotype development in the complement factor H mouse model of retinal degeneration but can be corrected by near infrared light.

Author information

1
Program of Neurosciences, Institute of Biology, Federal Fluminense University, Rio de Janeiro, Brazil; Institute of Ophthalmology University College London, London, UK.
2
Institute of Ophthalmology University College London, London, UK.
3
Moorfields Eye Hospital, London, UK.
4
Institute of Ophthalmology University College London, London, UK. Electronic address: g.jeffery@ucl.ac.uk.

Abstract

Mitochondria produce adenosine triphosphate (ATP), critical for cellular metabolism. ATP declines with age, which is associated with inflammation. Here, we measure retinal and brain ATP in normal C57BL/6 and complement factor H knockout mice (Cfh(-/-)), which are proposed as a model of age-related macular degeneration. We show a significant premature 30% decline in retinal ATP in Cfh(-/-) mice and a subsequent shift in expression of a heat shock protein that is predominantly mitochondrial (Hsp60). Changes in Hsp60 are associated with stress and neuroprotection. We find no differences in brain ATP between C57BL/6 and Cfh(-/-) mice. Near infrared (NIR) increases ATP and reduces inflammation. ATP decline in Cfh(-/-) mice was corrected with NIR which also shifted Hsp60 labeling patterns. ATP decline in Cfh(-/-) mice occurs before inflammation becomes established and photoreceptor loss occurs and may relate to disease etiology. However, ATP levels were corrected with NIR. In summary, we provide evidence for a mitochondrial basis for this disease in mice and correct this with simple light exposure known to improve mitochondrial function.

KEYWORDS:

670 nm; AMD; ATP; Aging; Retina

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