One of the more common theories of the aging process proposes that aging is attributed to the accumulation of damage to cell processes combined with the failure of protein synthesis to keep up with replacements. A bit of research published in the journal Cell Reports seems to be challenging that idea, thanks to the exploration of a long-lived mutant with a doubled lifespan. The catch? It’s a worm that normally lives about two weeks.
In Brief: Protein Synthesis and Protein Turnover
The so-called “protein turnover hypothesis” has been one train of thought among various anti-aging researchers. The idea is relatively simple, even if the underlying science is more complicated:
- As various molecules and proteins in cells accumulate damage, they will eventually reach a point where the body can’t resynthesize replacement proteins fast enough
- This leads to a buildup of damaged proteins, and causes cells to decline and die, thus being one of the primary causes of aging
- Therefore, increasing the degradation (removal) of damaged proteins and the synthesis of replacements (“protein turnover”) would slow down the aging process
And Now, Worms
All of this brings us to C. elegans, a tiny roundworm that has a maximum lifespan of about two weeks. Several years ago, a mutation was found that could cause elegans to live for roughly four weeks, though the molecular mechanism for this isn’t known. The researchers took some of the high life-expectancy worms and looked at their rates of protein turnover to see if it could confirm the hypothesis. If correct, they expected to see higher rates of protein degradation and new protein synthesis.
Interestingly, the researchers found the opposite: most proteins had slower synthesis and degradation rates in the mutant worms. No signs of increased turnover were observed, which may call in to question the hypothesis. While it is undeniable that protein damage and cellular degradation occur in the aging process, it may not be the primary cause.
What This Means
Unless you’re a worm farmer—it’s a thing—or an aging researcher, then these findings likely don’t mean much. Protein synthesis is a complicated affair and a lack of high protein turnover in worms with doubled lifespan isn’t enough to discount the hypothesis outright. It suggests that there’s more to learn and some prior assumptions that may need revisiting, but the findings also need verification and replication as well.
Dhondt, I., et. al., “FOXO/DAF-16 Activation Slows Down Turnover of the Majority of Proteins in C. elegans,” Cell Reports, 2016; http://dx.doi.org/10.1016/j.celrep.2016.07.088.
“Decelerated protein synthesis and degradation in a worm with doubled lifespan,” Alpha Galileo web site, September 14, 2016; http://www.alphagalileo.org/ViewItem.aspx?ItemId=167901&CultureCode=en, last accessed September 15, 2016.