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

@entity32 @entity71324 @entity19 @entity1457 @entity18458 @entity1020 @entity855
UNASSIGNED: Mitochondria produce @entity855 ( @entity855 ), critical for cellular metabolism. @entity855 declines with age, which is associated with @entity32 . Here, we measure retinal and brain @entity855 in normal C57BL/6 and complement factor H knockout @entity19 ( @entity71324 (-/-)), which are proposed as a model of age-related @entity1020 . We show a significant premature 30% decline in retinal @entity855 in @entity71324 (-/-) @entity19 and a subsequent shift in expression of a @entity1457 protein that is predominantly mitochondrial ( @entity18458 ). Changes in @entity18458 are associated with stress and neuroprotection. We find no differences in brain @entity855 between C57BL/6 and @entity71324 (-/-) @entity19 . Near infrared (NIR) increases @entity855 and reduces @entity32 . @entity855 decline in @entity71324 (-/-) @entity19 was corrected with NIR which also shifted @entity18458 labeling patterns. @entity855 decline in @entity71324 (-/-) @entity19 occurs before @entity32 becomes established and photoreceptor loss occurs and may relate to disease etiology. However, @entity855 levels were corrected with NIR. In summary, we provide evidence for a mitochondrial basis for this disease in @entity19 and correct this with simple light exposure known to improve mitochondrial function.
