By Liv Rowland, Nice, journalist, individual member of International Longevity Alliance

The event (geniilongevity.com) was organised by the International Longevity Alliance at Geneva’s International Conference Centre, near the United Nations’ European offices. It was IRCAN’s first presentation at an ILA event since joining as a federated member of the alliance of 74 organisations in 65 countries, who all hope to help build a world where healthy longevity is widely accessible through innovative medical technologies.

The main organiser, ILA chairman Dr Ilia Stambler, said: “I am happy that our conferences take place, making an additional good contribution toward international promotion of healthy longevity research, development and education, and international longevity community building. 

Opening the conference, dedicated to advancing longevity and optimising healthspan, Dr Dominik Thor of the Geneva College of Longevity Science, explained how Switzerland was chosen as the location as it is known for good healthcare and “is becoming a real hub for longevity”.

He added: “There are others in the world, and every one has distinct properties. Some people argue that one thing that may be holding us back here is conservative guidelines on regulatory policies compared to some other markets, such as in Asia, but this also stems from our belief in medicine based on rigorous clinical evidence, which is also very important for our patients.”

Dr Bulavin, one of the keynote speakers, told attendees how Nice is aiming to become such a hub.

“We are trying to build and enlarge the aging community here in Nice,” he said. “We are moving towards improving our median lifespan and also our healthspan, but one problem is that our absolute lifespan stands – as it was 100 years ago – at 120 years.”

He added: “We want to combine our basic research with clinical research and so we are in the process of creating a federation where we will try to make this transition more smooth. A lot of clinicians are very interested in such collaborations.”

He said data from humans shows a clear link between advancing age and likelihood of death, however there are some animal species where this correlation does not exist.

“If we can identify the mechanisms present in these species, we will be able to bring down the probability of death in humans and extend our healthspan to at least 120 years, but invariably, probably, extension of healthspan will push our lifespan as well.”

Traditionally, in anti-aging medicine, researchers seek to identify ‘hallmarks of aging’ – common biological features observed across species, thought to drive the aging process – and try to inhibit or reverse them. However, it is unclear how many would need to be dealt with to delay or reverse aging, and it may be a “daunting task”, Dr Bulavin told attendees.

That is why alternatives are emerging, ranging from “disruptive approaches such as four-factor partial reprogramming [of cells] to identifying the adaptive mechanisms of the body [that help it to maintain function despite the aging process]. Manipulating the latter, for example activating them earlier in life, may be an “accessible” way to delay aging in a “sustainable, efficient” way, including in poorer countries, he said.

“It could be simple medicine which could be injected or taken as a pill.”

A new social equation: global aging and inequality

Also among the speakers was Dr Alejandro Bonilla Garcia, an actuary and chair of the NGO Committee on Aging – which advocates for integration of aging in UN policies and programmes. He spoke of the need for social security systems to adapt to lowering fertility and a longer after-work period of life.

“We need a new social equation,” he said. “For decades were have been struggling with the fact of the shrinking rate of active people to inactive people, and now it’s shrinking more. With longer lives we need more economic efficiency. We have to rethink work, education and retirement and we have to agree on how we are going to do it at global and national levels.”

He added: “Some countries are getting smart and are really active and moving towards enhancing and innovating in longevity. They will benefit. Some countries are in a transition and others are lagging behind.”

Countries with effective social protection are those whose populations will be most able to benefit, he said.

He also told how the UN Human Rights Council has adopted a resolution to start drafting a convention on the rights of older persons.

“There is now a group of countries and UN agencies working on how we can have a legally-binding instrument. It’s not just about having people living longer, but also with rights and eliminating obstacles.

“We hope the process will continue into 2026 and countries will adopt this convention so that people who are extending and improving their lives and benefiting from longevity will be a wider group.”

The role of healthy lifestyles, and future funding

Several speakers stressed the importance of healthy lifestyles as a preventative measure. Start-ups presented ideas including apps optimising nutrition, memory retention or coping with chronic pain.

Dr Anna Erat, a medical expert from the University of St Gallen, Switzerland, stated: “We think about 80% of premature death from all causes can be prevented by healthy lifestyle and environment.”

She spoke of therapies being developed, such as using stem cells – especially pluripotent cells harvested from a person’s own body and specially treated – or others using NAD+ (a molecule involved in cell energy and repair) or DHEA (a hormone that supports various body functions and tends to decline with age), as well as use of health monitoring devices.

“How will be pay for this? By 2050, 2 billion people will be 60+. This is a problem in many countries but also an opportunity: 85-90% of healthcare expenditure goes to chronic disease management; if we can shift only a fraction into the healthy part of society, we can potentially save a lot of money.”

A lot of preventative medicine is not reimbursed, she said.

“We are not doing enough lobbying. If we want this to be a proper movement, we need to start, also for regulations to allow proper reimbursement, so we can scale and democratise longevity and ensure as many people as possible profit from it.

“Unfortunately, for now, most of the longevity medicine I do is paid for out of people’s pockets, but let’s try to change that.”

Longevity science: opportunities and gaps

Joshua Ferring, CEO of Longevity Science Foundation, a US grant-making non-profit which looks at what longevity research needs to be done, and where there are funding gaps, said: “We know a lot about longevity but there is so much more we don’t know, relative to what we do know, and that’s a problem.

“We need to talk about what needs to happen globally, not just in Switzerland, but across the entire world, to move us forward to a place where we are actually providing healthy longevity for people. Not just those with extreme financial means, but truly everyone.”

He added: “There is so much money in this industry right now. Lots of investment goes into various companies, but not enough into research.”

How IRCAN is changing the field of cellular senescence

In his presentation, Dr Bulavin also expanded on IRCAN’s work in cellular senescence, in which he and his team have shown the complexities of this process, where cells cease to divide, but do not die.

They have been long to contribute to the aging process – and are identified as a ‘hallmark’ – but IRCAN has shown how they also play protective and healing roles, so any approach to removal must be selective. In this sense, they are among adaptive mechanisms which could be harnessed for their benefits.

“If you look at factors considered positive or detrimental, the list of each is almost as long,” Dr Bulavin said. “For example, in young and middle age, cellular senescence often acts as a tumour suppressor or in wound healing and has a role in the innate immune response. However, in older age, it is often linked to sterile inflammation and tissue dysfunction.

“So, a potential approach is not to kill all detrimental cells, but rather to reverse them back to a beneficial state. And we need drugs that can target detrimental cells, but not affect beneficial ones.”

IRCAN’s research has also shown the types and interactions of senescent cells to be more complex than previously thought.

“This means we need to understand which one is doing what, and we need specific tools to identify these different cells and determine what role they play.”

IRCAN has been focusing on p16-high cells, which in mouse experiments can be seen to build up along with aging, in major body organs. TLR7, a receptor that plays a role in the immune system, has been found an effective way to induce these.

Many of us were exposed to a “TLR7 activator”, when we took the Pfizer Covid vaccine, he said.

“So the question is, if we have been exposed to something that induces senescence in immune cells, is it detrimental or beneficial?,” he said.

In fact, his team’s research on mice has shown this to protect against several kinds of harm including from sepsis and radiation, as well as being very rapidly effective against Covid – the original aim.

“A mouse injected with the vaccine gets resistance to severe Covid three days afterwards, way before it starts developing inhibitory antibodies. So Pfizer have done a good job in protecting us, first from severe tissue damage and inflammation, which then gives us time to develop the antibodies,” he said.

Experiments with transfer of p16-high immune cells to mice that do not have these show similar protective effects, and only a small number of cells are required (which may be an advantage if this is used for future therapies).

Dr Bulavin’s team has now experimented with transfer of human p16-high immune cells into mice given a toxin.

“We are capable of protecting them from sepsis with this approach,” he said. “This is under patent. It’s very interesting and one direction we are taking is using it for resistant cancers and other kinds of severe tissue damage and inflammation.”

This could include heart attack and wound healing, for example after burns.

“We can either vaccinate and in this case protect from the appearance of a pathology or implement these cells when a pathology appears and also have a beneficial effect.

“The question now is whether any long-lived organisms, with low aging rates, are using these mechanisms to live longer. We believe one example is bats.”

They have now identified a kind of mouse in which they can activate these cells from an early age, to see if they live healthier and longer.

They are found to have little age-related frailty compared to a typical mouse, and to live a little longer, he said. They are now coupling this with another approach that lowers overall inflammation, and experiments are ongoing in Dr Bulavin’s lab in Nice.