Key Points
Why This Research Matters: The Global Challenge of an Aging Population
From Lab to Clinic: The Challenges of Developing Aging Treatments
Cellular Pathways of Lifespan Regulation: How Our Cells Age
Rejuvenating Aged Stem Cells: Repairing the Body's Building Blocks
Drug Discovery in Aging Research: New Strategies, Old Drugs, and Artificial Intelligence
What These Findings Mean for Patients
Study Limitations: What This Research Could Not Prove
Practical Recommendations for Healthy Aging
Frequently Asked Questions
Source Information

Key Points

Metformin, felodipine, rapamycin, and guanabenz are approved drugs being studied for repurposing as aging interventions.
Stem cell rejuvenation research targets blood, muscle, intestinal, and brain stem cells to restore the body's repair capacity.
Sex differences matter: reducing C/EBPβ-LIP extended lifespan in female but not male mice.
AI-generated a drug candidate for a fibrosis target in just 21 days, accelerating discovery.
No reliable aging biomarkers exist yet, and human clinical trials for geroprotectors are still lacking.

Why This Research Matters: The Global Challenge of an Aging Population

Our world is aging rapidly. An increasing aging population poses a significant challenge to societies worldwide. As people live longer, the burden of age-related diseases like heart disease, diabetes, dementia, cancer, and frailty continues to grow. To effectively treat these conditions, researchers need a better understanding of the molecular, cellular, tissue, physiological, psychological, and even sociological changes that occur as we age.

The field of aging research is expanding at an extraordinary pace, with major advances happening across many previously disconnected areas of science. Recognizing this potential, several major pharmaceutical, biotechnology, and consumer companies have made aging research a priority. They are building internal expertise, integrating aging research into traditional business models, and exploring new strategies to bring treatments to market.

To accelerate these efforts, the Center for Healthy Aging at the University of Copenhagen and the artificial intelligence company Insilico Medicine created a community of Key Opinion Leaders and launched an annual conference series called "Aging Research and Drug Discovery (ARDD)." The 6th annual meeting was held in Basel, Switzerland — the capital of the pharmaceutical industry — as part of the Basel Life Science Week. It was co-organized by Morten Scheibye-Knudsen from the University of Copenhagen and Alex Zhavoronkov from Insilico Medicine.

This meeting explored the latest aging mechanisms and new interventions for age-associated diseases. The 7th annual ARDD exhibition was already scheduled for September 2–4, 2020, in Basel, demonstrating the rapid momentum of this field.

From Lab to Clinic: The Challenges of Developing Aging Treatments

Although great progress has been made in understanding how aging works at the biological level, effective drug interventions are still missing for most age-related disorders. Dr. Nir Barzilai from the Albert Einstein College of Medicine in New York highlighted one fundamental issue: the traditional approach to medicine is "one disease, one drug." Targeting the aging process itself challenges this model and requires a complete shift in thinking.

The TAME Study: Testing Metformin to Target Aging

One of the most talked-about developments at the conference was the "Targeting Aging with Metformin" (TAME) study, driven by Dr. Barzilai. This landmark study may represent a proof-of-concept that could pave the way for clinical trials leading to healthy aging. Metformin is a drug already used widely to treat type 2 diabetes, and it has a remarkable track record in aging research:

Metformin has been reported to extend lifespan in animal studies
A retrospective clinical study on type 2 diabetes treatments linked metformin use to longevity
A recently published human clinical trial underlined its widespread effects, revealing gene expression changes in aging-linked metabolic and non-metabolic pathways

Dr. Barzilai emphasized that political attention needs to be strengthened by highlighting the clinical and economic benefits of aging interventions. However, he noted that no party will cover intervention costs without an indication — and for that, simple and reliable biomarkers (biological indicators of aging) are still lacking. This is a critical gap that needs to be filled.

Other Promising Drugs and Lifestyle Interventions

Dr. Brian Kennedy from the National University of Singapore summarized known lifestyle interventions and small molecules that have been shown to cause lifespan extension. His research group recently made an exciting discovery: α-ketoglutarate (also known as alpha-ketoglutarate), an intermediate molecule in the tricarboxylic acid (TCA) cycle — a key part of cellular energy production — increases the lifespan of mice.

Strikingly, the effect of α-ketoglutarate was even more profound on healthspan (the period of life free from disease) than on lifespan in mice that received the diet starting at the age of 18 months (roughly middle-aged in mice). Improved healthspan was indicated by decreased levels of inflammatory factors in the blood, as well as a decreased frailty index — a measure of overall physical vulnerability.

However, a crucial mystery remains: whether these aging interventions actually improve healthspan in humans is not always clear. More research is needed to bridge this gap.

The Dog Aging Project: A Bridge Between Mice and Humans

So how do we fill the gap between laboratory animal research — which has traditionally stopped at studies in mice — and human clinical trials? Dr. Matt Kaeberlein from the University of Washington in Seattle and colleagues several years ago initialized an innovative project: the dog aging project.

Companion animals like dogs offer a unique advantage as model organisms because they:

Age faster than humans, allowing researchers to observe aging processes more quickly
Have high genetic diversity, reflecting the diversity seen in human populations
Share a common environment with humans, making findings more applicable to real-world conditions

The dog aging project aims to investigate how genetic and environmental factors influence the life- and healthspan of domestic dogs. This is being done through surveys, DNA sequencing, blood biochemistry testing, and extensive "omics" data collection (the study of genes, proteins, and other biological molecules). The project also provides an opportunity to test aging interventions — the first being rapamycin, a drug that inhibits the mammalian Target of Rapamycin (mTOR) pathway, a master regulator of growth and aging.

Notably, the completed phase 1 of the rapamycin intervention trial in dogs revealed no side effects and improved cardiac (heart) function in treated dogs. This is an encouraging result that supports the feasibility of testing aging drugs in larger, longer-lived animals.

The SENS Approach: Focusing on Healthspan, Not Just Lifespan

Dr. Aubrey de Grey from the SENS Research Foundation in Mountain View, California, emphasized an important message: placing the focus on healthspan rather than lifespan will help rebut societal concerns about longevity investigations. He also discussed how age-related diseases — which become more prevalent as we get older — should be treated and explored differently than communicable (infectious) diseases.

He introduced the SENS Research Foundation's concept of "maintenance": targeting the mechanisms that mitigate cellular damage that accumulates during aging. Notably, treatments for age-related diseases directed by spinouts of the SENS Research Foundation aim to improve the healthspan of elderly people, with increased longevity considered a positive side effect rather than the primary goal.

Cellular Pathways of Lifespan Regulation: How Our Cells Age

Aging entails a functional decline of multiple cellular pathways that are required to maintain cellular homeostasis — the delicate balance that keeps our cells healthy. Several years ago, scientists classified nine hallmarks of aging: the key biological processes that change as we grow older. However, exactly how these cellular mechanisms are regulated and interconnected remains poorly understood. The conference featured several researchers shedding light on these questions.

The Nucleolus: A Cellular Stress Hub in Aging

Dr. Adam Antebi from the Max Planck Institute for the Biology of Aging in Cologne, Germany, provided fascinating insights into how the nucleolus — a structure inside the cell's nucleus where ribosomes (the protein-making machinery) are assembled — functions as a cellular stress signaling hub during aging.

Recent work from his group revealed a correlation between reduced nucleolar size, reduced expression of a protein called nucleolar fibrillarin, and extended lifespan in the microscopic roundworm C. elegans. In support of these observations:

A mutant strain called ncl-1 with enlarged nucleoli had a reduced lifespan in various genetic longevity models
Conversely, knockdown of nucleolar fibrillarin (which reduces its activity) reduced nucleolar size and extended lifespan

Alongside reduced nucleolar size, long-lived C. elegans genotypes showed decreased ribosome biogenesis (the production of ribosomes). Intriguingly, the same correlation between nucleolus size and lifespan was also observed in fruit flies (Drosophila), in mice, and in isolated muscle cells from elderly people who underwent a short-term period of reduced caloric intake combined with exercise.

Even more remarkably, the nucleolus appears to play a role in the immune system. The researchers observed decreased nucleolar size and fibrillarin expression upon bacterial infections, suggesting a connection between the nucleolus, protein quality control (called proteostasis), immune function, and the aging process.

MicroRNA mir-71: How the Brain Communicates with the Gut to Control Aging

Dr. Thorsten Hoppe from the University of Cologne presented his latest research on how microRNAs (tiny RNA molecules that regulate gene expression) control protein quality control and longevity.

His group used an in vivo reporter assay (a technique that allows scientists to visualize biological processes in living organisms) to identify protein degradation defects in C. elegans mutants that lack the microRNA mir-71. The study revealed that mir-71 regulates how worms perceive food odors. Specifically, it controls the expression of a molecule called tir-1 mRNA in specific olfactory (smell) neurons called AWC (amphid wing cell C) neurons.

When this pathway is disturbed, it leads to reduced protein quality control in the intestine and premature aging in the worms. This research highlighted a signaling axis between the brain and the gut in response to food odor — a mechanism that may be highly relevant for age-associated neurological disorders such as Parkinson's disease, where protein misfolding and clumping are central features.

C/EBPβ-LIP: A Potential Mimic of Caloric Restriction

Dr. Cornelis F. Calkhoven from the European Research Institute for the Biology of Ageing in Groningen, Netherlands, shared his latest research on a transcription factor (a protein that controls gene activity) called C/EBPβ-LIP, which is driven by the mTORC1 nutrient-sensing pathway.

His group's research revealed that reduced expression of C/EBPβ-LIP in a mouse model resulted in:

Decreased age-dependent physical decline
Reduced immune aging
Lower tumor incidence
Improved metabolic function

Notably, increased lifespan was observed in female but not male mice — a sex-specific difference that highlights the complexity of aging biology.

In an effort to translate these findings into treatments, the researchers used a compound library of FDA-approved drugs in a luciferase-based reporter assay (a technique using light-producing enzymes to measure gene activity) to identify drugs that reduce LIP expression. In the long term, pharmacological inhibition of LIP expression could potentially be used to mimic the beneficial effects of caloric restriction — without the need to actually restrict food intake.

Rejuvenating Aged Stem Cells: Repairing the Body's Building Blocks

Stem cells are the body's repair cells — they have the remarkable ability to divide and produce specialized cell types, allowing tissues to regenerate and maintain themselves. Stem cell exhaustion (the loss of these repair cells over time) is thought to be a common feature of the aging process in multiple tissues. Therefore, stem cell rejuvenation holds great promise for treating age-related disorders by boosting the body's own repair capacity.

Sirtuins: The Mitochondrial Checkpoint in Blood Stem Cells

Dr. Danica Chen from the University of California, Berkeley, highlighted the role of sirtuins, a family of NAD+-dependent protein deacetylase enzymes, as key players in the aging process and as promising targets for stem cell rejuvenation. Sirtuins were originally identified as proteins that increase lifespan in yeast. In mammals, the homologues Sirt2, Sirt3, and Sirt7 have been shown to be downregulated (reduced in activity) in aged hematopoietic stem cells (HSCs) — the stem cells that produce all blood cells.

Dr. Chen and her team uncovered a mitochondrial metabolic checkpoint guarded by sirtuins that ensures mitochondrial health in HSCs. This checkpoint becomes dysregulated in HSCs of old mice, resulting in loss of HSC maintenance due to activation of the NLRP3 inflammasome (an inflammatory protein complex). Strikingly, targeting the Sirtuins-NLRP3 signaling pathway improved the function and repair capacity of aged HSCs — a significant step toward using stem cell rejuvenation as a therapy.

Neuronal Stem Cells: Awakening the Sleeping Brain

Dr. Ana Martin-Villalba from the German Cancer Research Center in Heidelberg, Germany, introduced the audience to the world of neuronal stem cell regeneration. With age, the number of neuronal stem cells (NSCs) in the subventricular zone of the brain declines. Recently, Dr. Martin-Villalba's group revealed that a fast decline of all subpopulations of NSCs occurs from young to middle-aged mice; however, in old mice, the decline slowed down.

Most importantly, the remaining population of neuronal stem cells is maintained in a resistant, quiescent (sleeping) state by inflammatory signals. Yet once these old NSCs are activated, they show functional similarity to young NSCs. This finding highlights the potential of NSC reactivation in the aged brain to counteract age-related neurological decline.

Muscle Stem Cells and the WISP1 Secret

Dr. Jerome Feige from Nestlé Research in Lausanne, Switzerland, discussed strategies for enhancing the repair capacity of aged muscle stem cells. Loss of muscle mass and function can begin as early as the young adult stage and can lead to a condition called sarcopenia — the age-related loss of muscle mass and strength that contributes vastly to the diminished quality of life in elderly people.

The integrity of muscle stem cells is not only influenced by internal (intrinsic) mechanisms, but also by the diverse microenvironment that surrounds them, including cells called fibro-adipogenic progenitor cells (FAPs). Recent work from his group revealed that targeting the muscle stem cell "niche" (their supportive environment) is a promising intervention strategy. Specifically, transcriptome profiling (analyzing all gene expression) identified a protein called WISP1 — a matricellular protein secreted by FAPs — as an important factor for maintaining the integrity of muscle stem cells. The expression of WISP1 declines during age, and restoration of WISP1 expression counteracts the loss of muscle regeneration capacity.

Intestinal Stem Cells: The Notum Inhibitor ABC99

Dr. Pekka Katajisto from the Institute of Biotechnology at the University of Helsinki, Finland, and the Karolinska Institute discussed targeting the stem cell niche to rejuvenate intestinal stem cells (ISCs). These cells are supported by Paneth cells, specialized epithelial cells located in the stem cell niche of the intestine.

Research has shown that caloric restriction inhibits mTORC1 signaling in Paneth cells, which in turn promotes ISC function through a paracrine mechanism (cell-to-cell communication), thereby improving the regenerative capacity of the intestinal epithelium after irradiation in mice.

During aging, the functionality of both ISCs and Paneth cells decreases in humans and in mice. Dr. Katajisto's research revealed that this loss of function is partly caused by an increase in a protein called Notum, which is secreted by Paneth cells. Notum is a deacylase that inactivates Wnt ligands — signaling molecules that are essential for ISC maintenance and function.

Strikingly, a Notum inhibitor called ABC99 increased Wnt signaling in ISCs and restored the functionality of aged ISCs in vivo (in living organisms). This represents a concrete pharmacological strategy for rejuvenating the aged intestinal lining.

Drug Discovery in Aging Research: New Strategies, Old Drugs, and Artificial Intelligence

The conference also addressed the practical question of how to identify aging interventions. Two main strategies were discussed: de novo drug discovery (creating entirely new drugs) and repurposing existing drugs (finding new uses for drugs already approved for other conditions). In particular, repurposing FDA-approved drugs provides numerous advantages, including lower costs and a shorter timeline for the drug development pipeline.

A Brief History of Geroprotection

Dr. Alexey Moskalev from the Moscow Institute of Physics and Technology approached the question of whether aging drug discovery is becoming a reality. The concept of geroprotection (protecting against aging) is not recent — it received attention as early as the 1950s, when Denham Harman proposed the free radical theory of aging and the potential of antioxidants to slow aging. Since that time, more than 250 compounds have been shown to increase lifespan in aging model organisms by targeting cellular processes such as autophagy (cellular self-cleaning), cellular senescence (the state where cells stop dividing), and DNA repair.

As aging is a multifaceted process, recent studies indicate that a combined use of drugs leading to healthy aging may increase the benefit compared to single interventions. However, clinical trials for geroprotectors are still lacking due to the missing availability of reliable biomarkers and beneficial drug classification — the same challenge raised by Dr. Barzilai.

New Insights into mTOR and Leucine Sensing

Dr. David Rubinsztein from the Cambridge Institute of Medical Research at the University of Cambridge, UK, discussed the nutrient sensor mTOR — one of the first and best-studied aging targets. However, its regulatory mechanism is still not fully understood. Studying how mTOR is regulated may help identify new interventions in the future.

Recent work from Dr. Rubinsztein's group highlighted a specific regulatory mechanism: how the amino acid leucine imposes control on mTOR signaling. Interestingly, in most cell types they studied, this signaling pathway was driven by the leucine metabolite acetyl-coenzyme A (a molecule central to metabolism) and was independent of any leucine receptor identified so far. However, leucine sensing does appear to be mediated by leucine sensors in some cell types, like HEK293 cells, suggesting that different cells may sense leucine through different mechanisms.

Felodipine: A Blood Pressure Drug with Neuroprotective Potential

Dr. Rubinsztein also underscored the potential of drug repurposing for identifying autophagy inducers in brain disease. A screen for FDA-approved L-type calcium channel blockers (a class of drugs used for hypertension) identified felodipine as a strong autophagy inducer. Felodipine showed neuroprotective effects in a mouse model of Parkinson's disease at plasma concentrations similar to those seen in people taking the drug for high blood pressure.

Selective Phosphatase Inhibition: Enhancing Protein Quality Control

Dr. Anne Bertolotti from the MRC Laboratory of Molecular Biology in Cambridge, UK, discussed her research on selectively inhibiting phosphatases — enzymes that remove phosphate groups from other proteins — to enhance the protein quality control system in neurological disorders.

Her group identified that the drug guanabenz selectively inhibits a protein phosphatase called PPP1R15A. This inhibition prevents the dephosphorylation of a key molecule called elF2alpha. Prolonged activation of elF2alpha reduces ER-stress (endoplasmic reticulum stress) caused by misfolded proteins, by regulating the rate of protein translation and chaperone availability.

Based on the promising effects of guanabenz, its derivative Sephin1 was shown to prevent molecular and physiological changes in disease models of Charcot-Marie-Tooth 1B (a hereditary nerve disorder) and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease). To expand this approach, Dr. Bertolotti's group developed a platform to screen for additional phosphatase inhibitors. As a proof-of-concept, Raphin1 was identified as a novel PPP1R15B inhibitor that attenuates neurological decline in a Huntington's disease mouse model.

The cGAS-STING Pathway: A Target for Inflammation

Dr. Andrea Ablasser from the Global Health Institute at École Polytechnique Fédérale de Lausanne (EPFL) discussed the potential of targeting the cytosolic DNA sensing pathway called cGAS-STING in human disease. The cGAS-STING pathway triggers the inflammatory response when DNA is detected outside the nucleus (in the cytosol), making it a promising target for inflammatory diseases.

Her group identified C-176, C-178, and their derivatives as small-molecule inhibitors of STING. A three-month treatment with C-176 in a mouse model of inflammatory disease strongly reduced inflammatory parameters. Notably, targeting the cGAS-STING pathway may also be relevant for diseases driven by cellular senescence, as the cGAS-STING pathway was recently shown to be a crucial regulator of cellular senescence.

DNA Damage and DNA Repair: A Key to Longevity?

Dr. Morten Scheibye-Knudsen from the Center for Healthy Aging in Copenhagen highlighted the diversity of aging features, consistent with the complexity of the aging process. He presented evidence for a central role of DNA damage in aging:

Loss of DNA repair leads to premature aging syndromes
Novel data suggesting that stimulating DNA repair might significantly extend the lifespan of model organisms

Importantly, in collaboration with Insilico Medicine, his team discovered a wealth of small molecules able to stimulate DNA repair — another example of how artificial intelligence is accelerating the discovery of potential aging interventions.

LINE1 Retrotransposons: Jumping Genes as Drivers of Aging

Dr. Andrei Gudkov from the Roswell Park Comprehensive Cancer Center and its spinoff biotech company Genome Protection, Inc. (GPI) in Buffalo, NY, discussed his ongoing work on genotoxic stress (damage to genetic material) as a driver of cellular senescence and aging.

A recent study indicated that the reactivation of retrotransposable elements (sometimes called "jumping genes" — pieces of DNA that can move around the genome) may be a source of DNA damage during aging. Inhibition of LINE1-encoded reverse transcriptase (an enzyme these elements need to copy themselves) significantly reduced age-related systemic inflammation and the accumulation of DNA damage markers. This approach may provide a target for both anti-aging and anti-cancer interventions.

Dr. Gudkov also briefly discussed the challenge of assessing the health status of organisms such as mice. To simplify this, his team developed the physiological frailty index — a non-invasive method to determine the biological age of mice, similar to frailty assessments used in human geriatric medicine.

Prion Diseases: Lessons from Neurodegeneration

Dr. Adriano Aguzzi from the Institute of Neuropathology at the University of Zürich discussed the latest developments in the research of prion diseases. Prion diseases are a group of neurodegenerative disorders caused by the misfolding and aggregation of a normal protein called the prion protein (PrPC). Dr. Aguzzi shared recent results regarding the disease-causing mechanism and possible interventions. Notably, prion diseases share some clinical and molecular features with age-related neurodegenerative diseases such as Alzheimer's disease, meaning insights from prion research may inform the broader field of neurodegeneration.

Artificial Intelligence: The New Accelerator for Drug Discovery

Artificial intelligence, particularly deep learning techniques such as generative and reinforcement learning, is spearheading many drug discovery efforts. Dr. Quentin Vanhaelen from Insilico Medicine shared recent work demonstrating how AI for generative chemistry can drive rapid drug discovery.

As a point in question, his group demonstrated that effective drugs can be developed in just 21 days for a new target. Specifically, an effective inhibitor of discoidin domain receptor 1 (DDR1), a kinase target implicated in fibrosis (tissue scarring), was generated in this remarkably short timeframe.

Clearly, AI-driven discovery has now progressed to a level where small-molecule design can be done more rapidly and accurately than ever before. Generative chemistry technology, combined with other computational chemistry techniques, is being applied to develop specific and selective modulators for multiple targets implicated in aging and age-related diseases.

Additionally, researchers discussed how AI can help analyze gene expression data. Publicly available gene expression datasets can be combined with user-owned unpublished data to identify altered pathways and possible drug molecules from Insilico Medicine's pharmaceutical AI department. Notably, this toolset provides information about possible patents and other intelligence that could guide industries in decision-making regarding which specific small molecules to pursue.

What These Findings Mean for Patients

The research presented at the ARDD 2019 conference has several important implications for patients and the general public:

Drug repurposing is a viable path to aging therapies. The fact that drugs like metformin, felodipine, guanabenz, and rapamycin — all already used in humans for other conditions — show promise as aging interventions means the timeline for bringing treatments to patients could be significantly shorter than for entirely new drugs.
Sex differences matter in aging research. The finding that C/EBPβ-LIP reduction extended lifespan in female but not male mice underscores the importance of studying both sexes and developing sex-specific treatment approaches.
Stem cell rejuvenation could restore organ function. The discoveries around sirtuins in blood stem cells, WISP1 in muscle stem cells, the Notum inhibitor ABC99 in intestinal stem cells, and the activation of old neuronal stem cells suggest that future therapies may be able to boost the body's own repair systems.
Caloric restriction mimetics are on the horizon. Compounds that mimic the effects of caloric restriction (like the LIP-expression inhibitors) could offer the health benefits of fasting without requiring actual dietary restriction.
Artificial intelligence is accelerating discovery. The ability to generate effective drug candidates in 21 days means that treatments for age-related diseases could be developed much faster and at lower cost than traditional drug discovery, which typically takes 10-15 years.

Study Limitations: What This Research Could Not Prove

While the findings presented at ARDD 2019 are exciting, it is important to understand their limitations:

Animal studies may not translate directly to humans. Many findings were demonstrated in mice, worms (C. elegans), and flies. While these model organisms are invaluable for aging research, results in animals do not always predict outcomes in humans.
Human clinical trials are still lacking. As several speakers emphasized, no reliable biomarkers of aging are currently available, and clinical trials for geroprotectors (drugs that protect against aging) are still largely absent. The TAME study with metformin is designed to help address this gap but had not yet been completed.
Healthspan vs. lifespan distinction. Many interventions extend lifespan in animals, but whether they genuinely improve healthspan (years of healthy, disease-free living) in humans often remains unknown.
Sex-specific effects. The observation that some interventions affect male and female mice differently highlights that findings from one sex may not fully apply to the other.
This is a meeting report, not a peer-reviewed clinical trial. The information represents presentations and discussions at a scientific conference. Some studies described are early-stage, and many have not yet been published in full or replicated by independent research groups.

Practical Recommendations for Healthy Aging

While we wait for aging drugs to be developed and approved, the research presented at this conference reinforces several evidence-based practices that patients can consider today:

Consider a balanced, nutrient-dense diet. The research on caloric restriction and its mimics (α-ketoglutarate, C/EBPβ-LIP inhibition) suggests that what and how much we eat significantly influences aging processes. Consult with your healthcare provider before making any major dietary changes.
Engage in regular physical activity. The finding that muscle cells from elderly people who underwent short-term caloric restriction and exercise showed smaller nucleoli (associated with longevity) suggests that lifestyle interventions can have measurable effects at the cellular level.
Stay informed about clinical trials. Studies like TAME (metformin), the Dog Aging Project (rapamycin), and others are actively recruiting or analyzing results. Patients may wish to discuss participation in aging-related clinical trials with their healthcare providers.
Do not self-medicate with over-the-counter or prescription drugs for anti-aging purposes. Many drugs discussed at this conference (e.g., metformin, rapamycin, felodipine) are prescription medications with potential side effects. Long-term use for aging prevention has not yet been approved by regulatory bodies and should only be undertaken as part of clinical research.
Be skeptical of unproven supplements. Despite the promise of antioxidants first proposed in the 1950s, no anti-aging supplement has been rigorously proven to extend human healthspan. Focus on lifestyle interventions with solid evidence: healthy diet, exercise, sleep, and stress management.

Frequently Asked Questions

What is the TAME study and what does it test?

The TAME study, presented at the conference, tests metformin—a diabetes drug—as a possible way to target aging. It may provide proof-of-concept that targeting aging itself could lead to clinical trials for healthy aging. This study had not yet been completed at the time of the meeting.

What is the Dog Aging Project and why use dogs for aging research?

The Dog Aging Project studies how genes and environment affect lifespan and healthspan in domestic dogs. Dogs age faster than humans, have high genetic diversity, and share human environments, making findings more applicable. A first rapamycin trial in dogs showed no side effects and improved heart function.

What does it mean to repurpose existing drugs like felodipine or metformin for aging?

Drug repurposing means finding new uses for medicines already approved for other conditions. For example, felodipine, a blood pressure drug, showed neuroprotective effects in a mouse model of Parkinson's disease. Repurposing offers lower costs and shorter timelines than creating entirely new drugs.

Can artificial intelligence really design new drugs faster?

Researchers demonstrated that an effective inhibitor of a target called DDR1 was generated in just 21 days using AI-driven generative chemistry. This suggests drug candidates for age-related diseases could be developed much faster and at lower cost than traditional drug discovery, which typically takes years.

What are the limitations of the aging research findings presented at this conference?

Many findings come from mice, worms, or flies, and may not translate directly to humans. Human clinical trials for aging drugs are still lacking, and reliable biomarkers of aging are not yet available. The report itself is a meeting summary, not a peer-reviewed clinical trial.

Are there any drugs I should take now to slow aging?

No. The article advises against self-medicating with prescription or over-the-counter drugs for anti-aging purposes. Drugs like metformin or rapamycin have potential side effects, and long-term use for aging prevention is not yet approved by regulatory bodies. Lifestyle measures like healthy diet and exercise have solid evidence.

What lifestyle recommendations are supported by this research?

Research reinforces eating a balanced, nutrient-dense diet, since caloric restriction and compounds mimicking it influence aging. Regular physical activity is supported, as elderly people who did short-term caloric restriction and exercise showed cellular changes linked to longevity. Always consult your healthcare provider before major dietary changes.

I'm in my 60s and heard metformin and rapamycin might slow aging. Should I ask for a second opinion before asking my doctor to prescribe one for anti-aging?

No drug is approved specifically to slow aging in humans. Drugs like metformin and rapamycin extend lifespan in animals, but human clinical trials for these anti-aging uses are still lacking; the TAME trial testing metformin had not yet been completed. Reliable biomarkers of aging are unavailable, and animal results do not always predict human outcomes. Patients should not self-medicate with prescription drugs for anti-aging purposes. A second opinion can clarify whether an experimental intervention is appropriate or whether joining a clinical trial is a safer route. Diagnostic Detectives Network provides independent expert second opinions.

Source Information

This patient-friendly article is based on the following peer-reviewed research publication:

Original Title: Latest advances in aging research and drug discovery

Authors: Daniela Bakula, Andrea Ablasser, Adriano Aguzzi, Adam Antebi, Nir Barzilai, Martin-Immanuel Bittner, Martin Borch Jensen, Cornelis F. Calkhoven, Danica Chen, Aubrey D.N.J. de Grey, Jerome N. Feige, Anastasia Georgievskaya, Vadim N. Gladyshev, Tyler Golato, Andrei V. Gudkov, Thorsten Hoppe, Matt Kaeberlein, Pekka Katajisto, Brian K. Kennedy, Unmesh Lal, Ana Martin-Villalba, Alexey A. Moskalev, Ivan Ozerov, Michael A. Petr, Reason, David C. Rubinsztein, Alexander Tyshkovskiy, Quentin Vanhaelen, Alex Zhavoronkov, Morten Scheibye-Knudsen

Publication: AGING (Aging-US), Volume 11, Issue 22, pages 9971–9976 (November 21, 2019)

Article Type: Meeting Report (6th Annual Aging Research and Drug Discovery Conference, Basel, Switzerland, September 10–12, 2019)

DOI/Publisher: www.aging-us.com

This article is an open-access publication distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Note: This patient-friendly article was created to translate the original scientific meeting report into accessible language for a general audience. It does not constitute medical advice. Always consult with a qualified healthcare professional regarding any health concerns or before making changes to medications, supplements, or lifestyle.

Table of Contents