Cells are very dynamic entities. They don't sit still, and they and their components are constantly in a state of flux. A cell is a sack of things that can be listed, understood and counted, sure, but at any given moment in time numerous parts are being dismantled and new parts created from raw materials. Levels of proteins ebb and flow as they are formed and destroyed.
All of this dynamism places an interesting spin on attempts to understand and then repair aspects of aging that depend on malfunctioning cellular components. Within cells there exist a range of important structures called organelles, some of which number in the hundreds or thousands, such as mitochondria. These are themselves very dynamic entities, busy with the process of dividing, fusing, and exchanging proteins between one another. Damage in mitochondria is not a static thing, as those damaged proteins can be shared around, and damaged and undamaged mitochondria can fuse to create an organelle that works. The only forms of damage that can last are those that provide some survival advantage to a mitochondrion, such as the ability to evade cellular quality control mechanisms, or wherein the particular form of damage can overwhelm undamaged variants.
Most interesting of all cells can even pass around mitochondria, which is a great way for potentially harmful forms of persistent or replicating damage to spread and thus have a greater detrimental effect than would otherwise be the case. The present view of mitochondria in aging is that there are indeed forms of damage to mitochondrial DNA that cause dysfunction in mitochondrial function that is both harmful and leads to the spread of damaged mitochondria because they evade quality control mechanisms. Thus the damaged forms can divide and multiply to take over a cell - and if exported elsewhere they will take over that cell as well. This doesn't actually appear to happen to more than a small fraction of cells over a human life span, but that small fraction is enough to cause great harm to tissues, blood vessels, and more.
The research linked below is another reminder that mitochondrial biochemistry is complicated, delving further into how mitochondrial pass around between cells. In this case it definitely looks like a vector by which bad mitochondria of the sort we care about could spread more than they otherwise would. Any approach to repairing mitochondria in aged tissue must thus be sufficiently comprehensive to ensure that all these tricks have no effect: it cannot matter how dynamic or widely traveled a mitochondrion is, the treatment must either repair it along with all of its peers or destroy it, leaving none of the damage behind to spread once more.
It's broadly assumed that cells degrade and recycle their own old or damaged organelles, but [researchers] have discovered that some neurons transfer unwanted mitochondria - the tiny power plants inside cells - to supporting glial cells called astrocytes for disposal. The [findings] suggest some basic biology may need revising, but they also have potential implications for improving the understanding and treatment of many neurodegenerative and metabolic disorders.
"It does call into question the conventional assumption that cells necessarily degrade their own organelles. We don't yet know how generalized this process is throughout the brain, but our work suggests it's probably widespread. The discovery of a standard process for transfer of trash from neuron to glia will most likely be very important to understanding age-related declines in function of the brain and neurodegenerative or metabolic disorders. We expect the impact to be significant in other areas of biomedicine as well."
Mitochondria are organelles that perform many essential functions, including providing the energy to cells. Cells remove damaged mitochondria through a process called mitophagy. Mitophagy is considered a subset of a process called autophagy, by which damaged organelles are enwrapped and delivered to lysosomes for degradation. Implicit in the categorization of mitophagy as a subset of autophagy, which means "self-eating," is the assumption that a cell degrades its own mitochondria. However, we show here that in a location called the optic nerve head, large numbers of mitochondria are shed from neurons to be degraded by the lysosomes of adjoining glial cells. This finding calls into question the assumption that a cell necessarily degrades its own organelles.