Old drug Clioquinol may slow aging
An old gastrointestinal drug, Clioquinol, has been shown to inhibit the aging-associated protein CLK-1 and is showing promise for treating Alheimer’s, Parkinson’s, and Huntington’s diseases.
It’s always good when an old (and therefore out of patent) drug gets fresh life breathed into it, especially when it’s touted as a potential new anti-aging therapy. Clioquinol was used as an antifungal and antiprotozoal up until the ’60s when it was implicated in an outbreak of Subacute Myelo-Optic Neuropathy (SMON) in Japan and discontinued. This was despite the absence of a proper investigation into whether it was actually the cause.
Now, researchers at McGill University in Canada have discovered a possible mechanism for clioquinol’s recent implication with lifespan-extension. Dr. Siegfried Hekimi et al. from McGill’s Department of Biology reports that it interacts with the CLK-1 protein, potently inhibiting its activity.
Clioquinol has been shown recently in animal models to reverse the progression of Alzheimer’s, Parkinson’s, and Huntington’s diseases.
“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,” says Dr Hekimi.
CLK-1, which exists in yeast and other eukaryotes, has a human homolog COQ7 and it’s responsible for the biosynthesis of ubiquinone in the mitochondrial and other membranes.
Ubiquinone is a co-factor in a variety of cellular redox processes, including mitochondrial electron transport, and it’s often involved in processes that produce reactive oxygen species (ROS).
Defects of the gene that encodes CLK-1 apparently slow down a variety of developmental and physiological processes, including the cell cycle, embryogenesis, post-embryonic growth, rhythmic behaviors, and aging (see Felkai et al., 1999).
Dr. Hekimi speculates that metal chelation may be involved in the effect, given that clioquinol is a metal chelator, meaning that it binds to metal ions in the cell, inactivating them or leading to their removal. Whether or not this is true remains to be seen…
Regardless, it’s great to see that an effective and cheap inhibitor of CLK-1 has been found. Next we’d like to see animal tests, especially as to whether it extends maximum lifespan. If successful, my guess is that more potent versions that are new and patentable will be investigated and hopefully one day brought to market. In the meantime, I don’t know if I’m brave enough to start taking clioquinol, I’ll look further into it, but I suspect I will be waiting on further results before diving in.
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