Fight Aging!

I noticed a recent open access paper (in PDF format) that explains in a very readable fashion how the last few years of new research into mitochondria may imply changes for a few important details in the mitochondrial free radical theory of aging.

Mitochondria are organelles of eukaryotic cells that contain their own genetic material and evolved from prokaryotic ancestors some 2 billion years ago. They are the main source of the cell's energy supply and are involved in such important processes as apoptosis, mitochondrial diseases, and aging. During recent years it also became apparent that mitochondria display a complex dynamical behavior of fission and fusion, the function of which is as yet unknown. In this paper we develop a concise theory that explains why fusion and fission have evolved, how these processes are related to the accumulation of mitochondrial mutants during aging.

If you look back in the Fight Aging! archives, you'll find a layman's explanation of how degenerative aging is caused in part by accumulating mitochondrial mutations. Mitochondria go bad as a natural consequence of their operation, and if enough go bad in the right way, and manage to escape the natural recycling mechanisms of the cell, then they take over that cell - causing it to malfunction, damage its surroundings, and release harmful reactive molecules that are carried throughout the body. Given enough cells doing this, you will become frail and eventually die as vital systems in your body become too damaged to operate correctly.

In this, we're all in the same boat. The interesting part of this process is that mitochondria swarm around a cell in bacteria-like herds, but the real damage only starts after a cell is completely taken over by clones of one particular mutant form of mitochondrion - a different dysfunctional clone army for each dysfunctional cell, each based on a particular random set of mutations. The question all along has been how that clonal takeover happens, and here the researchers propose that fusion is the culprit:

Another important finding of recent years is that individual mitochondria do not exist as permanently distinct entities, as has long been believed, but instead form a dynamic network within which the mitochondria regularly exchange proteins, [mitochondrial] DNA, and lipids by rapid fusion and fission processes ... The fact that mitochondrial fusions do occur revives an earlier idea that the selection advantage of deletion mutants is their reduced size, which allows them to replicate faster ... we propose that mitochondrial fusion is the underlying mechanism that opens the door for the clonal expansion of mitochondrial deletion mutants.

Does this view, if accurate, change any of the existing approaches to dealing with mitochondrial mutation and its considerable consequences to our health and life span? Not really, though one might argue that it complicates the question of what actually happens under the hood during the delivery of new, undamaged DNA into a cell's mitochondria. The problem remains the damaged DNA, and the resulting absence of necessary protein cogs in the mitochondrial machinery of energy generation and other functions - so either deliver fixed DNA, or deliver the needed proteins, and the problem is solved.