Many of the methods by which aging can be modestly slowed in laboratory species are characterized by increased cellular housekeeping: more repair, more clearance of broken molecular machinery, more removal of metabolic waste. The extended life span produced by calorie restriction appears to depend on this increase: it doesn’t happen in mice in which housekeeping processes are disabled. Most of the work on cellular housekeeping in aging is focused on autophagy, responsible for removing protein aggregates and cellular structures. The proteasome is a part of a separate system of housekeeping that deals with broken or otherwise unwanted proteins. (Though it can be debated as to just how separate these two systems actually are in practice – everything inside a cell connects to everything else in some way).
With this in mind, I’ll point out a paper that caught my eye today, in which researchers genetically enhance proteasomal activity in a mouse model of retinal degeneration. They show that the mice are better able to resist the loss of retinal cells: the cells are more robust in the face of damaged and harmful proteins that accumulate either with age or because of inherited mutations that
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