Interviews of 2021: senescence, young blood and dog longevity

Five of our favourite interviews with some of the world’s leading researchers from across the aging field.

Earlier this week, we brought you some of this year’s interview highlights from interesting companies in the longevity world. But we don’t spend all our time focused purely on the commercial side of longevity, and the work that goes on in the labs at academic institutions all over the world is absolutely vital to our sector. Today we’ve picked out some of the interviews that we particularly enjoyed in 2021.

Young blood or old?

With much of the world focused on the potential of young blood to improve longevity, our interview with UC Berkeley professor Irina Conboy challenged that view. She’s well-qualified to do so, having worked in the lab that produced the seminal 2005 paper on heterochronic parabiosis reversing aging in mice.

The Conboy research group.

“We think that if you inject an old person with bodily fluids from a young person, nothing good will happen, unless there is a critical blood loss and a need for a transfusion,” she told us. “But if you can neutralise or remove some determinant proteins that are elevated in ways that become counterproductive, then that old person will become younger.”

Rather than using young or old blood, Conboy’s lab decided to simply dilute blood plasma using saline.

“We showed that by diluting young blood, nothing bad happened… But remarkably, we found that if you dilute old plasma by 50%, the old animals are robustly rejuvenated, more significantly than anything else that was tried before or concurrently.”

Urging caution on senolytics

Targeting senescent cells (old cells that don’t die off and build up in our bodies as we age) continued to be a hot topic in longevity this year – so much so, we even wrote a dedicated market report on it! But, with several companies now actively developing senolytic therapeutics that target and kill senescent cells, we spoke to Buck Institute professor Judith Campisi, one of the world’s leading authorities on senescence, to get her perspective.

Judith Campisi
“The first question we want to know is, are these different cell populations good or bad, or both?” she told us. “We just don’t know. We definitely want senolytics that hit the bad guys, and not the good guys – and we don’t have that yet. We don’t have that at all.

“The second thing we want to ask is, are they stable, do they always express the same genes? The answer to that, based on some early indications, is no – they’re changing over time. So this is tricky, this senolytic thing, because we still have this vast ocean of unknowing that we have to begin to fill in.”

Senescence and the immune system

But not everyone is taking a senolytic approach to killing off senescent cells, and our interview with University of Birmingham professor Janet Lord explored how her lab is looking how to get the immune system to do the job instead.

Janet Lord
“One of the big drivers of aging is this build-up of senescent cells in the body, which are highly pro-inflammatory,” she told us. “We know that there are mouse studies which have induced senescence only in T cells, and that was enough for the mice to develop multimorbid conditions and frailty. So we actually think that targeting the immune system may be enough – you may not even have to completely get rid of senescent cells elsewhere.”

“There are two types of immune cell – CD8 T cells and natural killer cells – whose job is to actually kill senescent cells. As you get older, those cells don’t work as well and can’t kill as well, so what we’re trying to do is to get them to kill senescent cells better. This may have other benefits, because their other jobs are to kill virus-infected cells and tumour cells. So it would have all-round benefits if we could improve their function.”

First ‘true’ clinical trial for longevity

In September, we caught up with University of Washington professor Matt Kaeberlein, widely respected for his work exploring mechanisms of aging to drive the discovery of interventions to improve human healthspan. He shared his progress on The Dog Aging Project, which aims to demonstrate that companion dogs can provide a compelling model for aging and age-related disease in humans, and has just started a clinical trial using rapamycin in healthy dogs.

“I say this is really, to the best of my knowledge, the first true clinical trial for aging or longevity, because this is a healthy aging study,” he told us. “The dogs can’t already have an age-related disease at the start of the study – this is really just to find out if we can maximise healthspan. I think this is the first clinical trial where lifespan in a healthy population is the primary endpoint.

“I think that it’s important to be doing these kinds of studies to start to move some of these interventions from the basic science, preclinical, world out into the real world. In my opinion, companion dogs are a really powerful way to do that, because you can get answers in a reasonable timeframe, and you can actually do true aging and longevity clinical trials, which is simply not feasible right now in people.”

We should also give a mention here to our interview with Celine Halioua about her company Loyal, which is developing therapeutics to improve the healthspan and lifespan of dogs.

Increased life expectancy is worth trillions

Of course, not everything relating to longevity is about biology, a point exemplified in our conversation with London Business School professor Andrew Scott. His paper with David Sinclair of Harvard Medical School, and Martin Ellison of the University of Oxford, calculated the economic value of increasing US life expectancy by ten years to be an eye-popping $367 trillion.

Andrew Scott
But one of the biggest learnings for Scott was just how important compressing morbidity is.

“Longer life is good, but making sure healthspan catches up with lifespan is staggeringly valuable,” he told us. “And that is why we should try to delay aging, because yes, you get a longer life, but you get it in better health.

“As you increase health relative to life expectancy, the more you want to live longer. If people are ill in their 80s, they don’t want to reach their 80s, but if people are well in their 80s, then they want to reach their 90s. So you get this virtuous circle effect that makes aging an unusual disease – the better we get at tackling it, the more we value further gains.”