A Drug to Treat Aging May Not Be a Pipe Dream

More incredible developments in biotech.

Scientists now have a good handle on what causes us to age, biologically speaking: The so-called “hallmarks” of the aging process range from damage to our DNA—the instruction manual within each of our cells—to proteins that misbehave because of alterations to their chemical structure. Most excitingly, we now have ideas of how to treat them.

By the end of 2023, it’s likely that one of these ideas will be shown to work in humans. One strong contender is “senolytics,” a class of treatments that targets aged cells—which biologists call senescent cells—that accumulate in our bodies as we age. These cells seem to drive the aging process—from causing cancers to neurodegeneration—and, conversely, removing them seems to slow it down, and perhaps even reverse it.

A 2018 paper showed that in experiments in which mice were given a senolytic cocktail of dasatinib (a cancer drug) and quercetin (a molecule found in colorful fruit and veg), not only did they live longer, but they were at lower risk of diseases including cancer, were less frail (they could run further and faster on the tiny mouse-sized treadmills used in the experiments), and even had thicker, glossier fur than their littermates not given the drugs.

There are more than two dozen companies looking for safe and effective ways to get rid of these senescent cells in people. The biggest is Unity Biotechnology, founded by the Mayo Clinic scientists behind that mouse experiment and with investors including Jeff Bezos, which is trialing a range of senolytic drugs against diseases like macular degeneration (a cause of blindness) and lung fibrosis. There are many approaches under investigation, including small proteins that target senescent cells, vaccines to encourage the immune system to clear them out, and even gene therapy by a company called Oisín Biotechnologies, named after an Irish mythological character who travels to Tir na nÓg, the land of eternal youth.

Senolytics aren’t the only contenders, either: Others currently in human trials include Proclara Biosciences’ protein GAIM, which clears up sticky “amyloid” proteins, or Verve Therapeutics’ gene therapy to reduce cholesterol by modifying a gene called PCSK9. The first true anti-aging medicine will very likely target a specific age-related disease driven by a particular hallmark, rather than aging writ large. But the success of a drug targeting an aspect of aging in clinical trials will allow us to consider this loftier goal in the not-too-distant future.

In 2023, early success of these treatments could kickstart the greatest revolution in medicine since the discovery of antibiotics. Rather than going to the doctor when we’re sick and picking off age-related problems like cancer and dementia in their late stages when they’re very hard to fix, we’ll intervene preventively to stop people getting ill in the first place—and, if those treadmill-shredding mice are anything to go by, we’ll reduce frailty and other problems that don’t always elicit a medical diagnosis at the same time.

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Hey mate,
do you think we can profit from one of those developments in the sense that it might also provide treatment for PFS? Or did you just post it to illustrate how crazy the pharma industry has become? :sweat_smile:

Related:

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I think it’s encouraging to see the progress being made in the realm of regenerative medicine, base editing, CRISPR, epigenetic editing etc.

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Time is definitely on our side and I’m quite amazed by the rate of progress.

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Things do look promising with CRISPR. However, as you’ve mentioned many times, we need the research to rapidly accelerate. We won’t be able to get grant funding until causation is proven. Too many men have had their lives ruined or even lost from these drugs, and it’s evident that the mechanisms of action are the same for each of the post-drug conditions. It’s sickening. We need an out from this hell…

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Absolutely. We desperately need to set a faster pace. It’s definitely within reach, we just need more resources. That’s all it boils down to.

What makes the situation all the more frustrating, albeit also hopeful, is that the scientists do fundamentally believe it is fixable. A software, rather than a hardware, problem. We have a very solid initiative starting this year. But I have seen rare disease communities with far fewer sufferers, sometimes less than 100, raising on average a million a year for research. Surely we can match that.

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