Today, we take a look at three key emerging technologies that might add extra healthy years to your life by addressing the aging processes directly to prevent or delay age-related diseases.

Senolytics – Removing aged dysfunctional cells to promote tissue regeneration

As we age, increasing amounts of our cells enter into a state known as senescence. Normally, these cells destroy themselves by a self-destruct process known as apoptosis and are disposed of by the immune system. Unfortunately, as we age, increasing numbers of these cells evade apoptosis and linger in the body.

These senescent cells do not divide or support the tissues of which they are a part; instead, they emit a range of harmful chemical signals. Their presence causes many problems, including impairing tissue repair and increasing inflammation, and is linked with the progression of osteoarthritis[1-2], atherosclerosis[3], cancer[4] and other age-related diseases.

As if that was not bad enough, the harmful signals created by senescent cells can also encourage other nearby cells to also enter the same senescent state.

It has long been suggested that removing these problem cells could be a way to prevent or delay age-related diseases, and, indeed, positive results have been shown in mouse studies[5-7]. Therapies that remove senescent cells are commonly known as senolytics.

The SENS Research Foundation was one of the earliest proponents of removing senescent cells to promote tissue regeneration and to reduce inflammation. Other researchers have, in the years since then, begun to support this idea, with the key 2013 paper Hallmarks of Aging supporting the same approach[8]. This paper is widely supported in academia and has likely helped catalyse interest in the approach.

This interest has been ignited in the last year or so, with multiple groups working on senolytics in different ways. The leader of the pack is Unity Biotechnology, which is already beginning human clinical trials of senolytic drugs this year. Given that companies like Oisin and others are hot on the heels of Unity, we can probably be reasonably confident that this technology could be available in the next few years once passing through the clinical trial process, assuming all goes well.

DNA Repair – Repairing the damaged genome

As we age, our DNA becomes damaged, and the resulting genomic instability is considered by many researchers to be a key reason we age. Somatic cells are constantly exposed to a range of sources of DNA damage, from reactive oxygen species to UV radiation and environmental mutagens. DNA serves as a production plant for proteins, the small building blocks of the cell. When DNA gets damaged, some proteins can stop being produced or become misfolded, which, in turn, compromises the function of the cell.

When there are many cells with this kind of damage in the organs, important body functions can start to deteriorate. To cope with this constant assault, the body has developed a complex network of repair and maintenance systems that remove damage and repair the DNA. This system also includes mechanisms to maintain the integrity of mitochondrial DNA (mtDNA)[9].

It is important to note that this genomic damage is largely random in nature. Factors contributing to the loss of genomic stability are varied, and the kinds of effects they have are broad, such as somatic mutations, chromosomal aneuploidies, mutations and deletions in aged mtDNA, and defects in the nuclear lamina. All these things are part of the loss of genomic stability via damage to the DNA and mtDNA. The most well-known consequence of genomic instability is cancer.

Finding ways to repair our DNA and boosting that repair seems to be solid directions of research. This could plausibly be achieved by finding drugs that boost the repair systems we already have, augmenting our cells to repair DNA more efficiently or even repairing the genome directly using CRISPR or other gene-editing technologies.

Dr. David Sinclair and his team recently concluded a study in which they showed how nicotinamide adenine dinucleotide (NAD) facilitates DNA repair. The results of the study were very positive, and human clinical trials are set to begin this year to see if the results translate to humans.

While this is a less sophisticated approach than professor George Church’s proposal of boosting DNA repair by using genetic engineering to increase NAD in cells, it is still a potential route to helping us repair aged and damaged DNA. It is especially interesting as it is a technology we could be using in the near future, while gene editing and other more robust approaches pass through the approval process.

Stem Cells – Replacing lost cells to improve tissue repair and organ function

Stem cell transplants have been with us for more than a decade, and researchers have been using them to a lesser or greater level of success, depending on the application. Most readers have heard of and are familiar with these therapies.

Our bodies are populated with stem cells in various tissues and organs, and these stem cells are responsible for creating replacement cells and maintaining and repairing the tissues in which they reside. As we age, the supply of stem cells dwindles, and tissue repair and upkeep starts to fail; this is known as stem cell depletion and is one of the hallmarks of aging[10].

Stem cell therapies aim to improve tissue and organ function by replacing lost stem cells with transplants of new stem cells where they are needed. Since the 1980s, researchers have been attempting to perfect stem cell therapy and have met with varied success.

One of the challenges to overcome is that as we age, it becomes increasingly harder to encourage stem cells to survive and join the patient’s tissue; this is, in part, due to aged people having more chronic inflammation, which damages stem cells.

Science is steadily finding solutions to this problem, including regulating local inflammation at the treatment site, using biogels to protect stem cells transplanted into the patient, and examining more novel approaches to improve stem cell survival and efficiency. We have recently seen a dramatic improvement in age-related frailty thanks to stem cell therapies in senior citizens, and the news is frequently announcing similar progress.

Perhaps the most intriguing recent development in stem cell therapy is the idea that we do not even need to transplant stem cells from outside sources at all; instead, we can reprogram our own resident cells to become the cell types we need. Our cells are rigidly set in what they are and the functions they perform; this is, generally speaking, a good thing, as it would be very bad indeed if heart cells forgot they were heart cells and decided to be bone cells instead!

However, we are finding that cells can be changed from one type to another through cellular reprogramming, and it is looking increasingly likely that we can even reprogram the cells in situ. This could potentially mean that we could change common cells into less common cells that begin to run out as we age. Imagine transforming blood cells into b cells to treat diabetes, turning scar tissue into healthy heart tissue[11] after a heart attack, replacing lost cartilage for knee injuries, and changing common brain cells into dopamine neurons for Parkinson’s[12].


The three approaches discussed here are what we consider to be near-term technologies that are all currently in human clinical trials. They represent a significant change in how medicine thinks about aging and disease; the focus here is shifting to prevention and repair over dealing with diseases as they appear and trying to compensate for them.

While there is still considerable research to be done before these things become commonplace and the standard of care, it is clear that this is the direction medicine is heading. Prevention is always better than cure, and so this shift in how we regard aging and its relation to age-related diseases is very welcome indeed. We look forward to the day when we can all benefit from these technologies for healthier and longer lives.


[1] Jeon, O. H., Kim, C., Laberge, R. M., Demaria, M., Rathod, S., Vasserot, A. P., … & Baker, D. J. (2017). Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment. Nature medicine, 23(6), 775-781.

[2] Xu, M., Bradley, E. W., Weivoda, M. M., Hwang, S. M., Pirtskhalava, T., Decklever, T., … & Lowe, V. (2016). Transplanted Senescent Cells Induce an Osteoarthritis-Like Condition in Mice. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, glw154.

[3] Childs, B. G., Baker, D. J., Wijshake, T., Conover, C. A., Campisi, J., & van Deursen, J. M. (2016). Senescent intimal foam cells are deleterious at all stages of atherosclerosis. Science, 354(6311), 472-477.

[4] Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010). The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression. Annual Review of Pathology, 5, 99–118.

[5] Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., Van De Sluis, B., … & van Deursen, J. M. (2011). Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature, 479(7372), 232-236.

[6] Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., … & O’Hara, S. P. (2015). The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging cell, 14(4), 644-658.

[7] Roos, C. M., Zhang, B., Palmer, A. K., Ogrodnik, M. B., Pirtskhalava, T., Thalji, N. M., … & Zhu, Y. (2016). Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice. Aging cell.

[8] López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. Cell, 153(6), 1194-1217.

[9] Kazak, L., Reyes, A., & Holt, I. J. (2012). Minimizing the damage: repair pathways keep mitochondrial DNA intact. Nature reviews Molecular cell biology, 13(10), 659-671.

[10] López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. Cell, 153(6), 1194-1217.

[11] Qian, Li et al. (2017) Single-cell transcriptomics reconstructs fate conversion from fibroblast to cardiomyocyte. nature 10.1038/nature24454

[12] di Val Cervo, P. R., Romanov, R. A., Spigolon, G., Masini, D., Martín-Montañez, E., Toledo, E. M., … & Sánchez, S. P. (2017). Induction of functional dopamine neurons from human astrocytes in vitro and mouse astrocytes in a Parkinson’s disease model. Nature Biotechnology, 35(5), 444-452.

About the author

Steve Hill

As a scientific writer and a devoted advocate of healthy longevity technologies Steve has provided the community with multiple educational articles, interviews and podcasts, helping the general public to better understand aging and the means to modify its dynamics. His materials can be found at H+ Magazine, Longevity reporter, Psychology Today and Singularity Weblog. He is a co-author of the book “Aging Prevention for All” – a guide for the general public exploring evidence-based means to extend healthy life (in press).

  1. November 18, 2017

    Waste proteins form and can’t be broken down. They form (combine) in the plasma and become too large, plaque, to be removed from the cells to be moved through the gates.

    • mm
      November 18, 2017

      Interesting, given there has recently been a demonstration in the UK of a drug that dissolves plaques in the arteries of mice. The SENS approach seeks ways to remove amyloids and plaques and given the evidence to date it seems very likely ones that work in humans exist. GAIM is another promising approach for PD and AL plaques and has enjoyed considerable success in preclinical testing thus far. Almost certainly there are small molecules out there that can break down misfolded proteins and now the race is on to find them.

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