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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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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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Occurrence and characterization of lipofuscin and ceroid in human atherosclerotic plaque.

This report appears to be a review of the prevalence of lipofuscin and ceroid in and around atherosclerotic plaque in humans. Interestingly, in a quick search about ceroid, I found a report of statin administration enhancing lipofuscin accumulation in the livers of animals. I wonder whether some findings of lipofuscin and ceroid may be confounded by the fairly widespread use of statins in older humans.
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Senescent fibroblasts drive ageing pigmentation: A potential therapeutic target for senile lentigo.

I thought "senile lentigo" was more or less caused by lipofuscin accumulation. I thought other names for it included "liver spots" and "aging pigment". This group reports that in humans, senescent cells accumulate at sites of age-related skin pigmentation (senile lentigo), and the skin can be lightened if senescent cells are "eliminated" using "radiofrequency". This last is also a remarkable observation; has anyone heard of this being used to "eliminate" senescent cells before? Apparently this group is using this method in humans.
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Glucosamine-Induced Autophagy through AMPK⁻mTOR Pathway Attenuates Lipofuscin-Like Autofluorescence in Human Retinal Pigment Epithelial Cells In Vitro.

While these experiments were done in cell culture, it seems noteworthy that glucosamine induced autophagy and "decreased lipofuscin-like autofluorescence in native photoreceptor outer segment-treated RPE cells". I tagged this paper with the topic "rapamycin" because I wonder whether it may have similar effects via its inhibition of mTOR and enhancement of autophagy.
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Young plasma reverses age-dependent alterations in hepatic function through the restoration of autophagy.

These researchers report interesting results of injection of young rat plasma injected into aged rats three times per week for 4 weeks. They reported that aging impaired autophagy, but it was significantly restored with these injections. Even lipofuscin and fibrosis were "significantly attenuated" with young plasma injections. Moreover, inhibition of autophagy could prevent these effects, suggesting that restoration of autophagy may be one important pathway of apparent rejuvenation in these experiments.
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