People often ask; “Aging is a natural process that has existed forever, so how can it be a disease?”

In fact, aging has not existed forever. The very first living cell came into existence on Earth approximately 4.5 billion years ago. This cell had the ability to divide an infinite amount of times and was the progenitor for every living organism that has existed. It displayed no aging process and in theory would not die until an environmental factor killed it.

A ‘germ line’ is the lineage of any living cell that can be traced back to the very first living cell in the series. Three billion years after the first living cell appeared, multicellular organisms came into being, from worms to human beings.

The germ line was passed down the generations but did not exhibit the aging process. It was only when certain cells strayed from the germ line and became afflicted with disease that they became unable to reproduce infinitely and therefore began to age.

The fact that a disease has existed in our genetic code for a very long time does not mean it is not a disease. Take haemophilia or cystic fibrosis for example, that have lurked in our genes for thousands of years. Diseases should be cured, and aging is no exception.




 Simply put, we age because our cells age. In 1961, scientist Leonard Hayflick discovered there was a limit to the amount of times a human cell could divide. After 70 divisions, a cell’s ability to divide slows down and eventually stops as it reaches a stage called cellular senescence. The younger a person, the greater number of times a cell is able to divide. In essence, there is a specific property of human cells that limits our lifespan.

Scientists have proposed that the reason a cell can only divide a limited number of times is rooted in DNA replication, the copying of the genetic material inside a cell. Over time, the enzymes that replicate a strand of DNA cannot replicate all the way to the end, causing the loss of some DNA.

Here’s an analogy: think of DNA as a long row of bricks. Imagine DNA replication as a bricklayer walking backwards laying a new layer of bricks on top of the first row. When he reaches the end of the wall, the bricklayer finds he is standing on the brick he’s supposed to replicate. Since he can’t put a brick down where his feet are, he steps back and falls of the wall, leaving the final brick bare, meaning the new row is shorter than the original row.  

In the same way, our DNA is unable to copy itself, and the new strand ends up shorter than the old strand.

Fortunately, we are born with long, repetitive sequences of DNA call “telomeres”. These telomeres can be found at the end of each of our chromosomes, and later on shorten during the DNA replication process.  

Telomeres are made up of units called nucleotides, arranged in a repeating sequence like beads on a string. This sequence is repeated hundreds of times in every telomere. Each time our cells divide, our telomeres become shorter. They shorten throughout our lifetime.

When we are first conceived, our telomeres are around 15,000 nucleotides long. Our cells divide rapidly in the womb and by the time we are born they are 10,000 nucleotides long. They shorten throughout our lifetime, and when our telomeres reach around 5,000 nucleotides long, we die of old age. The number of telomeres we have remaining can be measured from our blood cells.








Obviously, our bodies must be able to re-lengthen our telomeres or our egg and sperm cells would contain telomeres the same length as the rest of our bodies and we would give birth to children who were older than us. Humanity would die out in a generation or two.

However, our reproductive cells do not exhibit telomere shortening – in other words they are essentially immortal. They are our germ line, the same one that descends from the first living cell on this planet.

The reason for this is that our reproductive cells produce an enzyme called telomerase, which adds nucleotides to the end of our chromosones, lengthening our telomeres. Telomerase fills the ‘gap’ left by DNA replication. Using our analogy of the row of bricks, when the brick layer is unable to lay the last brick, telomerase is like an angel who flies in and puts the last brick in place.  

if we find the right compound, we can turn on telomerase in every cell in the body


So, can we insert the telomere gene into our cells and expand our lifespan?

The short answer is no. Inserting the genes into cells often causes cancer. If the gene is inserted into our chromosomes in the wrong place, it can turn on cancer-inducing genes which can be life threatening.

Luckily for us, the telomerase gene already exists in all our cells, because the DNA in every one of our cells is identical and contains the same genetic code. The reason most of our cells do not express telomerase is because the gene is repressed in them as it is bound by a protein.

It is possible to coax the repressor protein off the gene with a drug-like compound that prevents the repressor from attaching to the DNA. In theory, if we find the right compound, we can turn on telomerase in every cell in the body.

Compounds such as these have been recently discovered. Sierra Science has discovered over two hundred compounds in twenty-nine different drug families that induce the expression of telomerase in normal cells.




That leaves us with the trillion-dollar question: is telomerase the cure for aging? So far, the signs point to yes: telomerase is a very likely cure for aging.

In 1997, scientists inserted the telomerase gene into normal human skin cells grown in a petri dish. They observed that the cells became immortal: they were able to divide an unlimited amount of times. When they examined these “telomerised” cells, they found the telomeres didn’t just stop shortening, but actually got longer. Did this mean the cells were becoming younger?

Scientists then inserted the telomerase gene into human skin cells that had very short telomeres and grew the cells into the skin on the back of mice. The skin from cells that had not received the telomerase gene look and behaved like old skin. The skin from cells with the telomerase gene looked and behaved like younger skin. For the first time ever, scientists had demonstrably reversed aging in human cells.

 In 2008 scientists described creating clone mice from mouse cells containing the inserted telomerase gene. On average, these mice lived 50% longer than cloned mice created from cells that didn’t contain the inserted telomerase gene.




A cure for aging exists, and we at Libella Gene Therapeutics believe we have it. There is enough proof of concept that we can confidently say it is definitively possible. There is now no longer any serious debate on three points:

  1. We age because our cells age;

  2. Our cells age because they contain a clock of aging;

  3. That clock can be altered in a number of ways, even in a living human being.

  4. The telomere is that clock. Telomere shortening causes aging as we know it. Lengthen the telomeres, and we can prevent or reverse aging.

We believe we can prevent or reverse aging using a new gene-therapy developed by Dr. Bill Andrews at Sierra Sciences that uses the AAV Reverse (hTERT) Transcriptase enzyme (the "Libella Gene Therapy”). We strongly believe we can lengthen telomeres using our Libella Gene Therapy. Lengthening telomeres is the key to treating and possibly curing Alzheimer's disease and other age-related diseases. Libella's' gene delivery system has been demonstrated as safe, with minimal adverse reactions in over 186 clinical trials.

After hundred of years of searching for it, we now know exactly where the Fountain of Youth is. We can point to it on a map (a map which turned out to be a diagram of the human cell).