Today I’ll point out an open access review of what is known of the activities of lipofuscin in neurodegenerative disease. The central nervous system falters and runs awry with age, and some fraction of that decline can be attributed to the growing presence of lipofuscin in long-lived neurons. Lipofuscin is a poorly categorized mix of hardy metabolic waste, such as oxidized lipids and sugars, much of it resistant to the comprehensive toolkit of enzymes and waste management processes that cells are equipped with. There is some debate over whether or not cells could, if less impacted by aging, clear out their lipofuscin, or whether even young cells would be challenged to carry out that task. It is probably the case that accumulation in old cells is some mix of failed housekeeping and compounds that even adequate housekeeping would struggle with.
The SENS rejuvenation research programs class lipofuscin as a fundamental cause of aging, a distinguishing point of difference between old and young tissues that is created as a side-effect of the normal operation of healthy metabolism. The suggested approach for dealing with this problem is to search for enzymes in soil bacteria that can break down lipofuscin
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