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1.  Treatment with 670 nm Light Up Regulates Cytochrome C Oxidase Expression and Reduces Inflammation in an Age-Related Macular Degeneration Model 
PLoS ONE  2013;8(2):e57828.
Inflammation is an umbrella feature of ageing. It is present in the aged retina and many retinal diseases including age-related macular degeneration (AMD). In ageing and in AMD mitochondrial function declines. In normal ageing this can be manipulated by brief exposure to 670 nm light on the retina, which increases mitochondrial membrane potential and reduces inflammation. Here we ask if 670 nm exposure has the same ability in an aged mouse model of AMD, the complement factor H knockout (CFH−/−) where inflammation is a key feature. Further, we ask whether this occurs when 670 nm is delivered briefly in environmental lighting rather than directly focussed on the retina. Mice were exposed to 670 nm for 6 minutes twice a day for 14 days in the form of supplemented environmental light. Exposed animals had significant increase in cytochrome c oxidase (COX), which is a mitochondrial enzyme regulating oxidative phosphorylation.There was a significant reduction in complement component C3, an inflammatory marker in the outer retina. Vimetin and glial fibrillary acidic protein (GFAP) expression, which reflect retinal stress in Muller glia, were also significantly down regulated. There were also significant changes in outer retinal macrophage morphology. However, amyloid beta (Aβ) load, which also increases with age in the outer retina and is pro-inflammatory, did not change. Hence, 670 nm is effective in reducing inflammation probably via COX activation in mice with a genotype similar to that in 50% of AMD patients even when brief exposures are delivered via environmental lighting. Further, inflammation can be reduced independent of Aβ. The efficacy revealed here supports current early stage clinical trials of 670 nm in AMD patients.
doi:10.1371/journal.pone.0057828
PMCID: PMC3585189  PMID: 23469078
2.  Aged peripheral retinal lesions originating from the ciliary body sweep away the retinal pigmented epithelium 
Aims
To investigate age-related lesions in the far-anterior retina that migrate from the ciliary body (CB) and how they affect the neural retina and retinal pigmented epithelium (RPE).
Methods
One eye from three healthy subjects aged 87, 92 and 93 years were used. Retinae were photographed, embedded in resin and then sectioned at 2 μm.
Results
Multiple elliptically shaped lesions were present in the CB. Larger lesions extended into the peripheral retina. Lesions resulted from deposits that had lenticular qualities. These develop centrally along Bruch's membrane sweeping away the RPE, such that piles of RPE cells were present around the deposits that resulted in retinal atrophy. The internal composition of the deposits revealed large numbers of spherical bodies, unlike those seen in drusen. RPE cells adjacent to these deposits and their underlying lesions became highly irregular, with melanin granules spacing themselves out within the cell and adopting similar orientations. This is a highly distinctive feature.
Conclusions
These far-anterior deposits were different in nature from drusen in terms of morphology, composition and origin. They swept away the RPE, exposing the Bruch's membrane and isolating the retina, leading to atrophy. They appeared to originate from the CB and progressed centrally. The deposits may have developed from the ciliary muscle, which would account for their elongated orientation. Their impact on melanin distribution in RPE cells was unexpected and unusual, implying that they release a signal that influences melanin organisation.
doi:10.1136/bjophthalmol-2011-301273
PMCID: PMC3355342  PMID: 22426947
Lesions/deposits; far-peripheral retina; RPE; retina; ciliary body; degeneration; pathology

Results 1-2 (2)