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AI can tackle ageing’s true complexity

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A new study has demonstrated that artificial intelligence can be used not just to accelerate drug discovery, but to fundamentally transform how it’s done – by targeting the full complexity of biological ageing.

In a collaboration between Scripps Research and Gero, a biotechnology company focused on ageing, scientists developed a machine learning model trained to identify compounds that act across multiple biological pathways – a process known as polypharmacology.

Instead of seeking a single “magic bullet,” the system embraces ageing as a complex, multifactorial process – and finds drugs to match.

When tested in Caenorhabditis elegans, a widely used model organism in ageing research, the compounds extended lifespan in over 75 per cent of cases. One increased lifespan by 74 per cent, placing it among the most effective life-extending compounds ever recorded in this model.

“Traditional drug discovery obsesses over precision, aiming to modulate a single pathway with laser-like focus,” said Dr. Peter Fedichev, CEO of Gero.

“But ageing doesn’t work that way. It’s systemic, intertwined, and defies one-dimensional solutions. That’s what our approach embraces.”

Until recently, intentionally designing multi-target drugs was considered impractical across most areas of medical research due to the complexity involved and increased risk of side effects.

Such compounds were often discarded rather than developed. The research by Fedichev and Dr. Michael Petrascheck, professor at Scripps Research, demonstrates that AI can now navigate this complexity, making their research the first known example of AI successfully designing polypharmacological interventions for ageing – by intention, not chance.

“It’s not just an incremental step. This is a genuine step change,” said Petrascheck. “It shows that AI can help researchers tackle exponentially more complex biological questions than they could have unassisted.”

From a translational perspective, the findings lay the foundation for a new generation of therapeutics that act systemically, not in isolation.

“The main impact is on the future development of drugs that can extend lifespan and treat chronic, age-related diseases,” said Petrascheck.

“Intentional polypharmacology increases the likelihood of efficacy because ageing isn’t the failure of one system – it’s the gradual breakdown of many systems simultaneously.”

This research was conducted by Petrascheck’s laboratory at Scripps Research, with support from the National Institutes of Health. Fedichev and Gero contributed the AI algorithm, which identified and selected compounds for the study.

 

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Space station partnership for bioprinting research

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Starlab Space has announced a partnership with Auxilium Biotechnologies to advance 3D bioprinting in orbit.

Auxilium will provide orbital 3D bioprinting and biofabrication capabilities (manufacturing biological materials) aboard the Starlab space station to support research and development in regenerative medicine, implantable medical devices and tissue engineering.

Regenerative medicine uses the body’s own materials to repair damage or replace diseased tissue.

Auxilium’s proprietary AMP-1 3D bioprinter has demonstrated the mass production of implantable medical devices and other complex structures, such as perfusable blood vessels, in microgravity, the very low gravity environment in space, aboard the International Space Station.

In November 2024, Auxilium created tiny, functional blood vessels aboard the International Space Station using its AMP-1 platform.

These vessels, with wall thicknesses about the width of a human hair, were produced in under an hour, which is not possible on Earth, where the process requires more time, materials and complex steps.

With Starlab, Auxilium aims to accelerate translation from experimental biology to manufacturable products, positioning AMP-1 as what it describes as a production facility for the next generation of life science technologies in space.

“3D printing in microgravity enables tissue architectures and material properties not achievable under standard 1g manufacturing,” said Isac Lazarovits, director of engineering at Auxilium.

“This biomanufacturing facility on board the future Starlab space station will expand access to low Earth orbit, lower barriers for industry and academia, and enable high-impact research and manufacturing that will benefit Earth.”

Microgravity enables enhanced protein crystallisation for drug development, 3D cell growth and disease modelling that aims to better replicate human biology, and stem cell research with potential applications for treating conditions such as Parkinson’s disease, diabetes and Alzheimer’s. Stem cells are cells that can develop into different cell types.

“This partnership demonstrates Starlab’s commitment to fostering innovation in life sciences,” said Marshall Smith, chief executive of Starlab.

“By providing companies like Auxilium with the infrastructure to advance biomanufacturing in microgravity, we’re creating pathways for breakthrough therapies that will improve lives on Earth.”

Starlab’s design enables full certification and operation within weeks, according to the company, which says this minimises delays and maximises efficiency for payload customers.

Through joint venture partners, customers can conduct research on the International Space Station, with the aim of ensuring a seamless transition to Starlab for future work.

Starlab Space is a US-led global joint venture among Voyager Technologies, Airbus, Mitsubishi Corporation, MDA Space, Palantir Technologies and Space Applications Services, with strategic partners including Hilton, Journey, Northrop Grumman and The Ohio State University.

Auxilium Biotechnologies develops bioprinting and biomanufacturing solutions and implantable medical devices.

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Two teas or coffees a day could lower dementia risk, experts say

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People who drink two to three cups of coffee or tea daily have a lower dementia risk, new research suggests.

Health records for more than 130,000 people showed that over 40 years, those who routinely drank two to three cups of caffeinated coffee or one to two cups of caffeinated tea daily had a 15 to 20 per cent lower risk compared with those who went without.

The caffeinated coffee drinkers also reported slightly less cognitive decline, a measure of how thinking and memory deteriorate over time, than those who opted for decaf and performed better on some objective tests of brain function.

The findings suggest habitual tea and coffee drinking may be good for the brain, but the research cannot prove it, as caffeine drinkers may be less prone to dementia for other reasons.

The study was led by Yu Zhang, who studies nutritional epidemiology at Harvard University.

A similar link would arise if poor sleepers, who appear to have a greater risk of cognitive decline, steered clear of caffeine to get a better night’s rest.

“Our study alone can’t prove causality, but to our knowledge, it is the best evidence to date looking at coffee and tea intake and cognitive health, and it is consistent with plausible biology,” Zhang said.

Coffee and tea contain caffeine and polyphenols, plant compounds that may protect against brain ageing by improving vascular health and reducing inflammation and oxidative stress, where harmful atoms and molecules called free radicals damage cells and tissues.

Substances in the drinks could also work by improving metabolic health. Caffeine, for example, is linked to lower rates of type 2 diabetes, a known risk factor for dementia.

The researchers analysed records of 131,821 volunteers enrolled in two big US public health studies, the Nurses’ Health Study and the Health Professionals Follow-up Study.

Both took repeated assessments of the participants’ diets, dementia diagnoses, any cognitive decline they experienced and scores on objective cognitive tests for up to 43 years.

Overall, men and women who drank the most caffeinated coffee had an 18 per cent lower risk compared with those who had little or none, with similar results seen for tea.

The effect seemed to plateau at two to three cups of caffeinated coffee or one to two cups of caffeinated tea. No link was found between decaffeinated coffee and dementia.

Further work is needed to confirm whether the two drinks actually protect the brain.

Gold standard trials that randomly assign people to drink caffeinated or decaffeinated drinks for decades before checking for differences in dementia diagnoses are largely impractical.

However, studies could explore whether the drinks drive biological changes linked to brain function, which could be spotted in scans or other tests, Zhang said.

Naveed Sattar, a professor of cardiometabolic medicine at the University of Glasgow, said getting clarity would not be easy, not least because caffeine can have good and bad effects on the brain.

Tea and coffee both contain antioxidants that may be beneficial, and a caffeine boost can motivate people to work, learn and exercise.

In some people, caffeine raises blood pressure, a significant driver of dementia.

“Caffeine does a multitude of things, some which may be beneficial, some which may be harmful, and the net effect can never be estimated until you do a randomised trial,” Sattar said.

Researchers believe about half of dementia cases worldwide can be prevented or delayed by tackling factors such as obesity, smoking, excessive alcohol consumption, hearing loss and high blood pressure.

“Don’t think of coffee or tea as a magic shield,” Zhang said.

“I’d say maintaining a healthy lifestyle, getting regular exercise, having a balanced diet and getting good sleep are all important to get better brain health.”

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Genetic influence on lifespan underestimated by half

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People are twice as likely to inherit their lifespan as previously thought, new research suggests.

The genetic contribution to how long a person lives is around 50 per cent, based on health databases in Denmark and Sweden. This reflects heritability, the share of lifespan differences due to genes.

For decades, many scientists believed genes and ancestry accounted for between about 10 and 25 per cent of longevity.

The research was led by scientists at the Weizmann Institute in Israel, with the Karolinska Institute in Sweden and Leiden University.

The earlier underestimates arose from limited historic health and mortality data, where deaths due to war, infectious disease, risky or unsafe work, accidents, poor diet and lack of medical care were hard to separate in records.

“For many years, human lifespan was thought to be shaped almost entirely by non-genetic factors, which led to considerable scepticism about the role of genetics in ageing and about the feasibility of identifying genetic determinants of longevity,” said Ben Shenhar of the Weizmann Institute.

Environmental forces such as disease or living conditions can mask or confound potential genetic effects.

Hereditary causes of death, for those not killed first by external causes, mean “processes originating within the body, including genetic mutations, age-related diseases and the decline of physiological function with age.” the researchers said.

“If heritability is high, as we have shown, this creates an incentive to search for gene variants that extend lifespan, in order to understand the biology of ageing and, potentially, to address it therapeutically.” said Shenhar.

Other recent research has pointed to a potential role for taurine, an amino acid, in slowing the ageing process.

Scientists have also highlighted the bowhead whale’s 200-year lifespan, attributed to a cellular protein that may protect against carcinogenic mutations.

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