Researchers here demonstrate that delivery of humanin to aged mice can improve cognitive function. Humanin appears to trigger increased levels of autophagy, the collection of processes responsible for recycling damaged proteins and cell structures. Increased autophagy is associated with many of the approaches shown to modestly slow aging in short-lived species such as nematodes, flies, and mice. These approaches largely involve applying mild stress to cells, such as via heat, lack of nutrients, or other methods, or directly triggering the signals that normally result from such stress. Increased autophagy for some period of time is the primary outcome.
One of the more important mechanisms by which autophagy influences aging may be the removal of damaged mitochondria. Swarms of mitochondria act as the power plants of the cell, producing chemical energy store molecules, but their function degrades with age. This is in part a reaction to rising levels of cellular damage, but it is also the case that a tiny fraction of mitochondria can malfunction dramatically due to DNA damage. This leads to errant behavior in cells that can damage the tissue environment. Greater recycling of mitochondria appears to reduce their dysfunction in aging, though nowhere near as
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