“Ex vivo and in vivo analyses demonstrate an age-related increase in lipofuscin content, up until the age of about 70 years. Thereafter, lipofuscin levels plateau or even decline. The reason for this decline is not clear, but it may involve one or a combination of lipofuscin degradation routes, e.g., voiding into the extracellular space (as basal laminar deposits or precursor material to drusen) or association with melanosomes. Concomitant with the accumulation of lipofuscin granules are a decrease in melanosomes and an increase in melanolipofuscin granules.”