Bioviva offers gene therapy for a myostatin inhibitor (the specific gene is not disclosed), and it has been tried by one of the team members, experimenting on himself 5 years ago, with good results in a younger man.
In a 2012 paper by Blasco’s student Bruno Bernardes de Jesus, ordinary lab mice were given gene therapy with an “extra” telomerase gene spread to their cells by a genetically-engineered virus. the mice lived 13-24% longer, and the experimenters reported “remarkable beneficial effects on health and fitness, including insulin sensitivity, osteoporosis, neuromuscular coordination and several molecular biomarkers of aging.”
Their team includes
* a lab that provides genetically modified viruses with a gene payload, made to order. (This has now become a reliable and predictable technology.)
* A doctor who has experience with experimental gene therapy, and who had the courage to experiment on himself five years ago, with good outcome thus far.
* Sites in Colombia and Mexico where doctors will administer therapies for which there is not yet FDA approval.
* Most important, a Scientific Advisory Board that includes two of the most prominent, senior biochemists who developed the science of telomerase in the 1990s and before. They are Bill Andrews and Michael Fossel.
* What they offer is gene therapy with hTERT and a proprietary myostatin inhibitor “in the same family with GDF-11,” according to CEO Elizabeth Parrish.
Abstract – Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer
A major goal in aging research is to improve health during aging. In the case of mice, genetic manipulations that shorten or lengthen telomeres result, respectively, in decreased or increased longevity. Based on this, we have tested the effects of a telomerase gene therapy in adult (1 year of age) and old (2 years of age) mice. Treatment of 1‐ and 2‐year old mice with an adeno associated virus (AAV) of wide tropism expressing mouse TERT had remarkable beneficial effects on health and fitness, including insulin sensitivity, osteoporosis, neuromuscular coordination and several molecular biomarkers of aging. Importantly, telomerase‐treated mice did not develop more cancer than their control littermates, suggesting that the known tumorigenic activity of telomerase is severely decreased when expressed in adult or old organisms using AAV vectors. Finally, telomerase‐treated mice, both at 1‐year and at 2‐year of age, had an increase in median lifespan of 24 and 13%, respectively. These beneficial effects were not observed with a catalytically inactive TERT, demonstrating that they require telomerase activity. Together, these results constitute a proof‐of‐principle of a role of TERT in delaying physiological aging and extending longevity in normal mice through a telomerase‐based treatment, and demonstrate the feasibility of anti‐aging gene therapy.
SOURCES- Hplus magazine, EMBO Molecular Medicine, bioviva