Healthy-length telomeres are essential for your health
- Telomeres are DNA sequences at the end of each chromosome
- Telomeres protect every DNA tip by forming a loop
- Short telomeres result in non-functional cells
- Short telomere can’t form a loop
- Activates DNA damage response
- Chromosomes fuse
- Cell dies or senesces
- Organism ages
Telomeres are a biological clock
Telomeres shorten as we age, causing death and disease
TERT mRNA extends telomeres
People with healthy-length telomeres have longer healthspans
On average people with longer telomeres live longer than people with shorter telomeres, even controlling for smoking, blood pressure, cholesterol level, BMI, age, and gender (Rode, 2015). Short telomeres correlate with early death, hypertension, cardiovascular disease, cancer, chronic infection, diabetes (reviewed in Weischer, 2014), Alzheimer’s disease (Thomas, 2008), and risk of post-stroke dementia (Martin-Ruiz, 2006). In human twin pairs, the twin with the shorter telomeres is more likely to die first (Kimura, 2008).
Telomere extension in old normal mice improves multiple aspects of aging, including neurological function, strength, insulin levels, and IGF-1 levels, and extends lifespan by 24% (Jaskelioff, 2011; Bernardes de Jesus, 2012). Telomere extension rescues animal models of disease including liver disease and pulmonary fibrosis (Rudolph, 2000; Povedano, 2018).
Because of the abundant evidence that short telomeres are unhealthy or fatal, and that telomere extension improves health and reverses symptoms of aging, therapeutic telomere extension has been advocated since the last century.
It has been known for over 35 years that the enzyme telomerase extends telomeres. But it was only in 2013 and 2019 that inventions at Stanford University enabled safe, rapid telomere extension by delivery of mRNA (Ramunas, 2015).
mRNA reverses years of telomere shortening in hours
Nucleoside-modified mRNA encoding telomerase reverse transcriptase (TERT) can be used to extend telomeres in vitro or in vivo. TERT mRNA is translated into TERT protein, which goes to the nucleus, complexes with a template to form the telomerase enzyme. The TERT mRNA is degraded within hours, and the TERT protein is degraded within days, but during that brief time telomeres are extended rapidly, reversing years of telomere shortening in hours. The extended telomeres resume shortening immediately after treatment, important for safety.
Nucleoside-modified TERT mRNA increases telomerase activity in cells briefly (left). During this brief time telomeres are extended rapidly, by hundreds of base pairs (middle). This is the equivalent of reversing years of telomere shortening. The treated cells are able to divide more times, but are not immortalized. The amount of telomere extension depends on the dose of TERT mRNA (right). TERT mRNA treatment delays senescence, rejuvenates old cells, and keeps young cells young longer (Ramunas, 2015).
Stem cells naturally make TERT mRNA to extend their telomeres to stay functional. We’ve adopted this natural process. We use TERT mRNA as a therapy that we deliver to the body to reverse aging. It extends lifespan in mouse models of age-related diseases. We are moving TERT mRNA rapidly toward clinical trials.
We also offer TeloAid, which is TERT mRNA for research use to help other labs advance rejuvenation research as rapidly as possible.