TICK TOCK

The Scary Link Between Our Molecular Clocks and Alzheimer’s

It’s caught the attention of the Jeff Bezos-funded immortality lab.

When it comes to anti-aging science and research, there’s probably no topic more interesting than telomeres. There are caps at the end of chromosomes that act like the plastic bit at the end of a shoelace—keeping our genetic material from getting frayed or tangled. As we age and our cells divide again and again, however, telomeres get shorter and shorter each time. This shortening has been linked to dementia and other age-related conditions. That’s why some call telomeres our “molecular clocks,” ticking down until the inevitable.

Now researchers believe that shorter telomeres have been linked to signs of Alzheimer’s in brain scans. In a new study published Wednesday in the journal PLOS ONE, British scientists at the University of Oxford compared the length of telomeres to MRI scans of participants’ brains. They discovered that scans with longer telomeres typically showed healthier brains.

The findings suggest that the faster a brain ages, the shorter telomeres become. This link could potentially lead to the development of treatments for age-related neurodegenerative issues such as dementia and Alzheimer’s—but, interestingly, not stroke or Parkinson’s disease.

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“We found associations between telomere length, a marker of biological aging, and multiple aspects of brain structure,” the authors wrote. “This may explain why individuals with longer telomeres have a lower risk of dementia.”

The study’s authors looked at the MRI scans of more than 31,000 participants in the U.K. Biobank (an ongoing study of factors important to health and aging). They found that longer telomere length was generally associated with greater “grey matter volumes” in the brain, which also tends to decline with Alzheimer’s; and a thicker cerebral cortex, which typically thins with age.

This suggests that accelerated cellular aging might indicate a “biological pathway to neurodegenerative disease,” according to the study. Understanding this pathway requires more research, of course, but could be the key to creating new and more effective treatments for one of the most pernicious and devastating neurodegenerative diseases out there.

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It’s important to note, though, that the use of the U.K. Biobank might mean that there’s a healthy volunteer bias—which means that those who are most likely to volunteer for these studies are already going to be fairly healthy, and less likely to have issues like Alzheimer’s and shorter telomeres.

However, the new findings do offer some strong evidence that the genetic quirk of aging might play some factor in neurodegenerative issues. After all, there’s a reason why the Jeff Bezos-funded anti-aging venture Altos Labs is so interested in telomere length. If we can suss out the connection between shortening telomeres and cognition, we might be able to slow down—or even put a stop to—aging once and for all.

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