Lipofuscin[1], the age pigment, is produced in oxygen deprivation, apparently from reduced iron which attacks unsaturated fats. It has its own "respiratory" activity, acting as an NADH-oxidase.
Melanin is produced by polymerization of amino acids, with copper as the catalyst. With aging, iron tends to replace copper. Melanin is an antioxidant. Thus, there is a sort of reciprocal relationship between the two types of pigment.[2]
In cultured brain cells, it was found that vitamin E and ethyl alcohol promote its disappearance. (Where is this study mentioned by Ray?)
The hydroxyl-group on ethanol might be an radical scavenger and an anti-lipofuscin therapeutic at low doses
(1989) Effect of ethanol on lipofuscin accumulation in cultured rat cardiac myocytes https://www.sciencedirect.com/science/article/pii/0891584989901421 The 3.1 mM ethanol group performed better than higher concentrations in this study, equal to 0.14 g/L or 0.014 % = less than half a serving of alcohol for most people.
(1995) Radiosensitization and radioprotection of E. coli by alcohols https://pubmed.ncbi.nlm.nih.gov/7902388/
(1999) Is ethanol an important antioxidant in alcoholic beverages associated with risk reduction of cataract and atherosclerosis? https://pubmed.ncbi.nlm.nih.gov/10496411/
(1969) Lipofuscin (aging) pigment granules of the newborn human liver https://pubmed.ncbi.nlm.nih.gov/4182373/ Lipofuscin is found in fetal and newborn (!) liver. Here is evidence lipofuscin is not strictly a product of aging and perhaps it can be reversed.