Tinkering With CLK-1 to Slow Aging

CLK-1 - or clock-1 - is a gene that affects lifespan, most likely through its influence on mitochondrial activity. It's the standard story, or at least appears to be: anything that can lower the rate at which mitochondria damage themselves will extend life in flies, mice, and so forth. I noticed a piece today on a drug candidate for neurodegenerative diseases that researchers now think works through manipulation of CLK-1:

Recent animal studies have shown that clioquinol - an 80-year old drug once used to treat diarrhea and other gastrointestinal disorders - can reverse the progression of Alzheimer's, Parkinson's and Huntington's diseases. Scientists, however, had a variety of theories to attempt to explain how a single compound could have such similar effects on three unrelated neurodegenerative disorders.

...

"Clioquinol is a very powerful inhibitor of clock-1," explained Hekimi, McGill's Strathcona Chair of Zoology and Robert Archibald & Catherine Louise Campbell Chair in Developmental Biology. "Because clock-1 affects longevity in invertebrates and mice, and because we're talking about three age-dependent neurodegenerative diseases, we hypothesize that clioquinol affects them by slowing down the rate of aging."

...

Hekimi is optimistic but cautious when asked whether clioquinol could eventually become an anti-aging treatment.

"The drug affects a gene which when inhibited can slow down aging," he said. "The implication is that we can change the rate of aging. This might be why clioquinol is able to work on this diversity of diseases that are all age-dependent."

However, he admits to being concerned about how people may interpret his results.

"The danger is that you can buy a kilogram of this compound at a chemical wholesaler, but we don't want people to start experimenting on themselves. Clioquinol can be a very toxic substance if abused, and far more research is required."

Wait and see is a smart strategy in medicine so long as you have the time for that choice. This is a mechanism for affecting mitochondria that I haven't seen mentioned much in the past, and so a big dive into the unknown. Even if progress is made in manipulating it, I imagine we won't hear much on the development side for some years. Those of you interested in keeping your mitochondria in better shape would most likely be better off exercising and eating less in any case - even the current batch of potential mitochondria-affecting drugs don't do as well as calorie restriction and exercise combined.

Needless to say, the real solution to all this is not to dig up drugs that slow things down, but rather to develop processes that repair or replace damaged mitochondria and thus reverse this aspect of aging. Based on what has been taking place in laboratories over the past few years, this doesn't look to be any harder, and should be a lot more effective.

Comments

Post a comment; thoughtful, considered opinions are valued. Comments incorporating ad hominem attacks, advertising, and other forms of inappropriate behavior are likely to be deleted.

Note that there is a comment feed for those who like to keep up with conversations.