Aging has always occupied an unusual place in human consciousness. It is biological, but also existential. It is measurable in tissues and molecules, but also lived through memory, loss, maturity, dependence, wisdom, and decline. For centuries, aging has been understood as a natural part of the life course rather than as a discrete disease. Yet modern biotechnology, especially gene therapy and cellular reprogramming, has reopened the question. If aging can be slowed, repaired, or partially reversed at the molecular level, should it be classified as a disease?

The answer matters. To call aging a disease is not merely a semantic distinction. It changes how medicine defines health, how regulators approve therapies, how society allocates resources, and how human beings understand the final stages of life. The longevity movement argues that classifying aging as a disease could accelerate research and allow therapies to target the root causes of many chronic illnesses. This argument has practical force. Aging is the greatest risk factor for cancer, cardiovascular disease, dementia, frailty, and many other conditions. If medicine could intervene earlier in the biology of aging, it might prevent or delay multiple diseases at once rather than treating them one by one (Barzilai et al., 2016; WHO, 2025).

Yet the stronger position is that aging is a biological process, not a disease. Aging can increase disease risk without being a disease itself. It can produce vulnerability without being identical to pathology. It can be modified by medicine without being reclassified as an illness. This distinction is not semantic; it protects both scientific clarity and human dignity.

At the biological level, aging is the gradual accumulation of molecular and cellular changes over time. These include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, stem-cell exhaustion, altered intercellular communication, chronic inflammation, and other hallmarks now widely discussed in geroscience (López-Otín et al., 2013; López-Otín et al., 2023). These processes reduce resilience and increase disease susceptibility. However, they are not abnormal in the way that a cancer mutation, infectious invasion, autoimmune attack, or congenital enzyme deficiency is abnormal. They are part of the expected trajectory of living systems.

This is why the comparison with adolescence is useful. Adolescence involves dramatic biological changes: hormonal shifts, altered brain development, changing body composition, increased risk-taking, and heightened vulnerability to certain mental-health problems. Yet adolescence is not a disease. It is a developmental stage. We may treat complications that arise during adolescence, but we do not classify adolescence itself as pathology. Similarly, aging involves biological change and increased vulnerability, but that does not automatically make it a disease (University of Kansas Medical Center, 2024).

A disease is usually understood as a departure from normal biological function that affects some individuals or affects individuals in a way that produces identifiable pathology. Aging is different. It is universal among organisms that survive long enough. It is continuous with the rest of the development. It begins not as a sudden pathological event but as the later arc of biological life. Embryonic development, childhood growth, puberty, adult maintenance, reproductive decline, and senescence are all stages in one continuous process. To classify senescence alone as a disease risks creating an artificial boundary within the life course.

This does not mean aging is harmless. Aging is the background against which many diseases become more likely. Atherosclerosis, Alzheimer’s disease, osteoarthritis, sarcopenia, many cancers, and metabolic disorders all become more common with age. But calling aging a risk factor is different from calling it a disease. High blood pressure is a disease or clinical condition; age is a context in which risk accumulates. Smoking increases the risk of lung cancer, but smoking itself is not lung cancer. Aging increases the risk of dementia, but aging itself is not dementia.

Supporters of the disease model make a serious practical argument. If aging were recognized as a disease, drug development might become easier. Regulators could approve therapies that target aging biology itself rather than waiting for a specific disease endpoint. The Targeting Aging with Metformin trial was designed partly to test whether a drug might delay several age-related conditions together, thereby treating aging biology as a modifiable target even if aging is not formally classified as a disease (Barzilai et al., 2016; Barzilai, 2017). This is a reasonable scientific strategy. But it does not require the conclusion that aging is itself a disease. Medicine can target processes without redefining them as diseases. Inflammation, blood clotting, wound healing, puberty, pregnancy, menopause, and immune activation can all be medically managed in some contexts, but they are not automatically diseases.

This disagreement remains active in the scientific literature. Some authors argue that biological aging should be classified as a disease because it is harmful, progressive, and potentially modifiable, while others argue that the aging-disease distinction is more complex than either side admits (Bulterijs et al., 2015; Gems, 2015). This essay accepts the importance of targeting aging biology, but rejects the need to classify aging itself as a disease.

The current excitement around gene therapy makes this debate more urgent. Gene therapy strategies for age-related decline are no longer purely speculative. Reviews now describe approaches targeting telomerase, mitochondrial function, senescent cells, epigenetic regulation, DNA repair, metabolic signaling, and other pathways involved in aging and age-associated diseases (Jing et al., 2025; Shchukina et al., 2025; Yu et al., 2023). These studies show that mechanisms associated with aging are increasingly modifiable. They do not prove that aging, as a whole, is a single disease entity.

One of the earliest and most influential aging-related gene therapy studies used adeno-associated virus serotype 9 to deliver telomerase reverse transcriptase, or TERT, to adult and old mice. Bernardes de Jesus and colleagues showed that AAV9-mediated TERT gene therapy delayed several age-related changes and increased longevity in mice without increasing cancer incidence in that experimental setting. Mice treated at one year of age showed a greater lifespan benefit than very old mice treated at two years of age, suggesting that timing may matter (Bernardes de Jesus et al., 2012).

This study is important because telomere attrition is one of the recognized hallmarks of aging. However, it also illustrates the problem with calling aging a disease. Telomerase therapy did not “cure aging.” It modified one pathway associated with aging. Telomere shortening is one contributor to cellular decline, but it is not the whole of aging. Moreover, increased telomerase activity has theoretical cancer concerns because many cancers use telomerase to maintain replicative immortality. The mouse study was reassuring in its own context, but translation to humans remains uncertain.

A more controversial study was published by Jaijyan and colleagues in Proceedings of the National Academy of Sciences in 2022. The authors reported that mouse cytomegalovirus vectors carrying either TERT or follistatin could be delivered intranasally or by injection and could extend median lifespan in mice while improving several age-associated measures, including glucose tolerance, physical performance, body mass maintenance, alopecia, telomere shortening, and mitochondrial structure (Jaijyan et al., 2022). Because the reported lifespan effects were large, the study attracted attention in the longevity field.

However, this paper was later retracted in 2025. Therefore, it should not be used as positive evidence that CMV-based TERT or follistatin gene therapy extends healthy lifespan. Its proper place in this debate is as a cautionary example: aging-related gene therapy claims can be dramatic, commercially attractive, and scientifically exciting, but they must survive replication, data review, peer scrutiny, and long-term safety evaluation before being treated as reliable evidence (Retraction for Jaijyan et al., 2025). Including the retracted paper strengthens rather than weakens the argument for caution. The gene therapy field is promising, but promise is not proof.

The most scientifically dramatic aging-related gene therapy approach is partial cellular reprogramming. Full reprogramming with Yamanaka factors can erase cell identity and create pluripotent stem cells, but full reprogramming is dangerous in vivo because it can produce teratomas and loss of tissue identity. Partial reprogramming attempts to expose cells briefly or incompletely to reprogramming factors so that youthful epigenetic features are restored without erasing identity.

Ocampo and colleagues showed that cyclic expression of the four Yamanaka factors—OCT4, SOX2, KLF4, and c-MYC, collectively OSKM—ameliorated age-associated hallmarks in a mouse model of premature aging and improved tissue repair in normally aged mice (Ocampo et al., 2016). Because c-MYC increases oncogenic risk, later studies often removed it and used OSK instead of OSKM. Lu and colleagues used AAV2-mediated OSK expression in retinal ganglion cells and showed that reprogramming could restore youthful DNA methylation patterns, promote axon regeneration after optic nerve injury, and reverse vision loss in mouse models of glaucoma and natural aging (Lu et al., 2020). Yang and colleagues later argued that loss of epigenetic information may be a driver of mammalian aging and showed that OSK expression could reverse some aging-like changes in their inducible changes-to-the-epigenome model (Yang et al., 2023).

A more recent systemic study by Macip and colleagues delivered inducible OSK using adeno-associated viral vectors to very old mice. The study reported improved frailty scores and extension of remaining median lifespan in aged male mice (Macip et al., 2024). This is one of the strongest preclinical claims for gene-therapy-mediated partial reprogramming as a geroscience intervention. Even so, it remains animal evidence. It does not yet establish safety, durability, dose control, tissue specificity, or cancer risk in humans.

The most important current human translation of this concept is ER-100, developed by Life Biosciences. ER-100 is an AAV2-based gene therapy designed to deliver OCT4, SOX2, and KLF4. In 2026, Life Biosciences received clearance to begin a Phase 1 human trial of ER-100 for optic neuropathies, including open-angle glaucoma and non-arteritic anterior ischemic optic neuropathy (ClinicalTrials.gov, 2026; Life Biosciences, 2026a; Nature Biotechnology, 2026). In June 2026, Life Biosciences announced that the first patient had been dosed in the Phase 1 trial (Life Biosciences, 2026b). This trial made major news because it represents a formal clinical attempt to test an epigenetic-restoration strategy in humans.

The importance of ER-100 should not be understated. It is scientifically significant because it asks whether controlled partial reprogramming can be delivered safely to human tissue. If successful, it may open a path toward treating specific age-related degenerative conditions by restoring function rather than merely slowing decline. However, the trial must be interpreted carefully. ER-100 is not being tested as a general cure for aging. It is being tested for defined eye diseases involving optic nerve damage. The primary purpose of a Phase 1 trial is safety and tolerability, not proof of rejuvenation, lifespan extension, or reversal of human aging.

This distinction is central to the argument of this essay. ER-100 strengthens the scientific case that aging-related mechanisms can be modified. It does not prove that aging itself is a disease. The clinical indication remains glaucoma and NAION, not aging. Therefore, the trial supports a healthspan-oriented model—use gene therapy to treat specific age-related pathologies, reduce suffering, and preserve function, while avoiding the broader and philosophically unstable claim that normal aging is itself a disease.

A separate high-profile human episode often discussed in the same context is Elizabeth Parrish and BioViva. Parrish underwent experimental telomerase and follistatin gene therapies outside the United States in 2015 and later claimed biological-age-related improvements (Wired, 2017; Wired, 2023). This attracted substantial media attention because it was presented as one of the first attempts to use gene therapy against aging in a human. However, it was not a conventional, controlled, regulated clinical trial. It involved self-experimentation and later controversial clinical activity outside the usual standards of randomized, peer-reviewed, regulator-supervised medicine. For that reason, it should be discussed as a historically important and provocative episode, not as reliable evidence that human aging has been reversed.

Together, ER-100 and the BioViva episode show the two faces of the field. ER-100 represents the regulated path—defined disease indication, formal trial registration, dose monitoring, safety assessment, and regulatory oversight. BioViva represents the frontier path—bold, influential in public imagination, and important as a cultural moment, but scientifically limited because the evidence is uncontrolled and difficult to interpret. The future of aging-related gene therapy should follow the former model, not the latter.

Other gene therapy strategies reinforce the same lesson. Davidsohn and colleagues developed AAV-based therapies using fibroblast growth factor 21, alpha-Klotho, and soluble transforming growth factor beta receptor 2. These genes were tested individually and in combination in mouse models of obesity, type 2 diabetes, heart failure, and kidney disease (Davidsohn et al., 2019). The study was important because it suggested that secreted factors might influence multiple age-related disease pathways. But it also showed that combination therapy is not straightforward. Aging is not a single linear pathway, and adding more “beneficial” genes does not automatically produce more benefit.

FGF21 has also emerged as an important metabolic target. AAV-mediated FGF21 gene therapy has been shown to improve obesity and insulin resistance in mouse models, and later work has extended this approach to metabolic dysfunction-associated steatohepatitis and broader healthspan-related outcomes in aged animals (Jimenez et al., 2018; Jimenez et al., 2024; Jimenez et al., 2026). These findings are relevant because metabolic dysfunction is central to many age-related diseases. Yet again, the strongest conclusion is not that aging is a disease. The more precise conclusion is that age-associated metabolic decline may be modifiable.

Klotho is another longevity-associated target. AAV9-mediated delivery of secreted Klotho has been reported to improve physical function, muscle features, bone parameters, and neurological resilience in mice (Roig-Soriano et al., 2025). Similarly, work on longevity-associated variants such as LAV-BPIFB4 suggests that genetic variants found in exceptionally long-lived humans may influence vascular, immune, cardiac, and frailty-related aging phenotypes in animal models (Cattaneo et al., 2023; Ciaglia et al., 2022; Giuliani et al., 2023). These studies are exciting because they suggest that biological resilience may be transferable or therapeutically enhanced. But they remain preclinical.

Sarcopenia, the age-associated loss of skeletal muscle mass and function, is another area where gene therapy may become relevant. Ozes and colleagues tested AAV1-mediated neurotrophin-3 gene therapy in aged wild-type mice and reported improvements in muscle physiology, endurance, peripheral nerve myelination, and neuromuscular junction connectivity (Ozes et al., 2023). Follistatin gene therapy has also been studied in muscle-disease contexts such as Becker muscular dystrophy, where early human work showed encouraging safety and functional signals in a small trial (Mendell et al., 2015). These interventions are relevant to frailty and muscle decline, but they are still best understood as tissue-specific or disease-specific approaches, not as cures for aging itself.

Progeria illustrates the distinction especially well. Hutchinson-Gilford progeria syndrome is a rare genetic disorder caused by pathogenic changes in LMNA that produce progerin, leading to features of accelerated aging in children. It is rare, pathological, and clearly disease-causing. Gene-editing approaches in mouse models have shown that correcting the underlying mutation can improve vascular pathology and extend survival (Koblan et al., 2021). More recent work has explored longevity-associated variants such as LAV-BPIFB4 in progeria-related cardiac aging models (Qiu et al., 2025). These studies justify treating pathological acceleration of aging. They do not prove that normal aging is a disease. Rather, they show the opposite: disease is what happens when the normal process is distorted, accelerated, or made catastrophic by a specific pathological cause.

Even cross-species longevity-gene transfer supports the same careful interpretation. Naked mole-rats are exceptionally long-lived rodents with unusual resistance to cancer and age-related decline. Zhang and colleagues generated transgenic mice expressing the naked mole-rat hyaluronan synthase 2 gene, nmrHas2, and reported improved healthspan and modest lifespan extension (Zhang et al., 2023). This was not a conventional adult human gene therapy study. It was a genetic model showing that longevity-associated adaptations from one species can influence healthspan in another. It belongs in the scientific discussion of aging biology, but it should not be mistaken for clinical proof that normal human aging has been therapeutically reversed.

The existence of an intervention does not prove that the thing being modified is a disease. We can use growth hormone in specific disorders without calling childhood a disease. We can treat menopausal symptoms without calling menopause itself a disease. We can perform cataract surgery without claiming that aging, as a whole, is pathological. In the same way, gene therapy may one day treat age-related blindness, frailty, immune decline, metabolic disease, or neurodegeneration without requiring us to call aging itself a disease.

The classification question also has ethical consequences. If aging is called a disease, then every older person becomes, by definition, diseased. Wrinkles, slower gait, gray hair, reduced fertility, diminished muscle mass, and changing memory could all be framed as symptoms. This risks medicalizing the entire human life course. It may also worsen ageism by implying that older bodies are defective bodies. The World Health Organization has explicitly clarified that ICD terminology should not be interpreted as classifying old age itself as a disease (WHO, n.d.). The controversy over “old age” in ICD-11 showed how sensitive this issue is: the language was revised after concerns that it could pathologize age and reinforce social prejudice (Rabheru et al., 2022).

There is also a resource-allocation problem. If aging becomes a disease, should society prioritize expensive anti-aging interventions over childhood vaccination, maternal health, infectious disease control, disability care, or basic access to medicines? Advanced gene therapies are likely to be expensive at first. If they are framed as treatments for the “disease” of aging, they may deepen inequality by giving the wealthy access to biological maintenance unavailable to the poor. The goal of medicine should be not merely longer survival for those who can pay, but broader healthspan, function, independence, and dignity across populations.

A better framework is to treat aging as a modifiable biological process and age-related diseases as legitimate medical targets. This preserves the value of geroscience without collapsing process into pathology. It allows researchers to study the mechanisms of aging, identify biomarkers of biological age, and test interventions that delay disease or preserve function. It also allows clinicians to treat cancer, dementia, frailty, osteoporosis, sarcopenia, immune decline, macular degeneration, and cardiovascular disease without declaring the whole aging person diseased.

This balanced approach also aligns better with human experience. Many people do not want aging to be “cured” in the abstract. They want to remain mobile, lucid, connected, useful, and free from avoidable suffering for as long as possible. They want healthspan, not merely lifespan. They want dignity, not denial. Medicine should help people age well, not teach them that aging itself is a personal failure or a biological defect.

The future of aging research is promising. Gene therapy, senolytics, epigenetic reprogramming, metabolic interventions, regenerative medicine, and better preventive care may transform late life. These advances should be pursued seriously, but with conceptual humility. Aging is not simply an enemy to be defeated. It is the biological cost of being alive, reproducing, repairing, adapting, accumulating experience, and existing in time.

Therefore, aging should be understood as a natural biological process that can become the soil from which disease grows. The diseases should be treated. The suffering should be reduced. The decline should be delayed where safely possible. But aging itself should not be reduced to pathology. To do so would mistake universality for abnormality, vulnerability for disease, and human finitude for medical failure.

The wiser goal is not to cure aging, but to understand it—not to deny mortality, but to improve the years we have. Not to medicalize old age, but to protect health, function, independence, and dignity throughout the natural arc of life.

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