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Lipofuscin-dependent stimulation of microglial cells.

With this study being in cell culture, I have doubts about its relevance to the development of human age-related macular degeneration. But his group reported that microglia "quickly and completely" phagocytosed lipofuscin, and this was associated with "highly elevated levels of pro-inflammatory cytokines...in the cell culture supernatants". They go on to suggest perhaps this interaction between microglia and lipofuscin might be a cause of inflammation and angiogenesis in AMD.
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MicroRNA-29 enhances autophagy and cleanses exogenous mutant αB-crystallin in retinal pigment epithelial cells.

From this report, it appears that miR-29 may have an important role in regulating autophagy, at least in RPE cells in cell culture. This group reported that miR-29 overexpression increased autophagic activity, but from the abstract, they apparently didn't observe a reduction in lipofuscin or drusen--something they said they tried to find. But they did note that miR-29 overexpression "enhances autophagy which aids in the removal of protein aggregates".
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Recombinant Manganese Peroxidase Reduces A2E Burden in Age-Related and Stargardt’s Macular Degeneration Models.

Here, Kelsey Moody and his colleagues report on some proof-of-concept experiments that I and others worked on in the context of AMD. Their results include that recombinant manganese peroxidase, when produced in Pichia pastoris, is mannosylated and can degrade A2E and other fluorophores in vitro. Interestingly, this recombinant enzyme can also "reduce the A2E burden when administered by intravitreal injections in vivo".
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Quantitative Fundus Autofluorescence in Non-Neovascular Age-Related Macular Degeneration.

I found this report remarkable because this group found that control participants had *lower* fundus autofluorescence than all patients with AMD (< .001). I thought I read (maybe I'm wrong) that autofluorescence was a decent marker of "junk" accumulation that was associated with AMD, and this report contradicts that idea. The authors say something to this effect in their conclusion: "suggesting that loss of lipofuscin fluorophores, not increase, signifies AMD progression."
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Oxysterol Signatures Distinguish Age-Related Macular Degeneration from Physiologic Aging.

This group reports that oxysterols, especially 24-hydroxycholesterol, were associated with AMD in human peripheral blood mononuclear cells. Perhaps age-related changes in macrophage processing of cholesterol may be the cause of an elevation of oxysterols during aging (presuming there is one)? Or maybe this age-related change in cholesterol processing causes a greater predilection for atherosclerosis in later years?
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