Scientists at the European Molecular Biology Laboratory and the University of Rome have identified a protein called mlGF-1 that induces stem cells from other parts of the body to migrate quickly to muscles damaged from disease or injury. Our ability to produce mlGF-1 declines with age, but this age-related process can be reversed by administering the protein. This may be a key step in stem cell therapy.
Even more exciting is the prospect of replacing one's organs and tissues with their "young" replacements without surgery. Cloned telomere-extended cells introduced into an organ will integrate themselves with the older cells. Through repeated treatments over a period of time, the organ will end up being dominated by the younger cells. We normally replace our own cells on a regular basis anyway, so why not do so with youthful telomere-extended cells rather than older telomere-shortened ones? There's no reason why we couldn't eventually do this with every organ and tissue in our body. We would thereby grow progressively younger.
covered and named nanog by a team at the Institute for Stem Cell Research in Edinburgh.26 "Nanog seems to be a master gene that makes embryonic stem cells grow in the laboratory," says Ian Chambers, one of the teams scientists. "In effect this [gene] makes stem cells immortal." The insight is a big step in being able to turn any cell, such as a skin cell, into a pluripotent cell, which can then be transformed into any other type of cell.
Our understanding of the principal components of human ageing is growing rapidly. Strategies have been identified to halt and reverse each of the ageing processes. Perhaps the most energetic and insightful advocate of stopping the ageing process is Aubrey de Grey, a scientist with the department of genetics at Cambridge University. De Grey describes his goal as "engineered negligible senescence"—stopping us from becoming more frail and disease-prone as we get older.27
According to de Grey, "All the core knowledge needed to develop engineered negligible senescence is already in our possession—it mainly just needs to be pieced together."28 He believes we'll demonstrate "robustly rejuvenated" mice—mice that are functionally younger than before being treated, and with the life extension to prove it—within 10 years, and points out that this demonstration will have a dramatic effect on public opinion. Showing that we can reverse the ageing process in an animal that shares 99 per cent of our genes will profoundly transform the common wisdom that ageing and death are inevitable. Once demonstrated in an animal, robust rejuvenation in humans is likely to take an additional 5 to 10 years, but the advent of rejuvenated mice will create enormous competitive pressure to translate these results into human therapies.
Earlier in the evolution of our species (and precursors to our species), survival was not aided—indeed, it would have been hurt—by individuals living long past their child-rearing years. As a result, genes that supported significant life extension were selected against. In our modern era of abundance, all generations can contribute to the ongoing expansion of human knowledge. "Our life expectancy will be in the region of 5,000 years ... by the year 2100," says de Grey. By following the three bridges described in this book, you should be able to reach the year 2100, and then, according to de Grey, extend your longevity indefinitely.
De Grey describes seven key ageing processes that currently encourage senescence and has identified strategies for reversing each. Here are four of de Greys key strategies:
Chromosomal (nuclear) mutations and "epimutations."29 Almost all of our DNA is in our chromosomes, in the nucleus of the cell. (The rest is in the mitochondria, which we'll come to in a moment.) Over time, mutations occur, that is, the DNA sequence becomes damaged. Additionally, cells accumulate changes to "epigenetic" information that determine which genes are expressed in different cells. These changes also matter because they cause cells to behave inappropriately for the tissue they're in. Most such changes (of either sort) are either harmless or just cause the cell to die and be replaced by division of a neighbouring cell. The changes that matter are primarily ones that result in cancer. This means that if we can cure cancer, nuclear mutations and epimuta-tions should largely be harmless. De Grey's proposed strategy for curing cancer is pre-emptive: it involves using gene therapy to remove from all our cells the genes that cancers need to turn on in order to maintain their telomeres when they divide. This will not stop cancers from being initiated by mutations, but it will make them wither away before they get anywhere near big enough to kill us. Strategies for deleting genes in this way are already available and are rapidly being improved.
Toxic cells. Occasionally, cells get into a state where they're not cancerous, but still it would be best for the body if they died. Cell senescence is an example, and so is having too many fat cells. In these cases we need to kill those cells (which is usually easier than reverting them to a healthy state). Methods are being developed to target "suicide genes" to such cells, and also to make the immune system kill them.
Blocking the telomerase enzyme is one of many strategies being pursued against cancer. Doing this would prevent cancer cells from replicating more than a certain number of times, effectively destroying the cancers ability to spread. There are many other strategies being intensely pursued to overcome cancer. Particularly promising are cancer vaccines designed to stimulate the *
immune system to attack cancer cells. These vaccines could be used to prevent cancer, as a first-line treatment, or to mop up cancer cells after other treatments.30 We'll discuss Bridge Two strategies against cancer in more detail in chapter 16, "The Prevention and Early Detection of Cancer."
Mitochondrial mutations. Another ageing process identified by de Grey m is accumulation of mutations in the 13 genes in the mitochondria, the energy factories for the cell.31 The mitochondrial genes undergo a higher rate of mutations than those in the nucleus and are critical to the efficient functioning of our cells. Once we master somatic gene therapy, we could put multiple copies of these 13 genes within the relative safety of the cell nucleus, thereby providing redundancy (backup copies) for this vital genetic information. The mechanism already exists in cells for nucleus-encoded proteins to be imported into the mitochondria, so it is not necessary for these proteins to be produced in the mitochondria itself. In fact, most of the proteins needed for mitochondrial function are already coded by the nuclear DNA. There has already been successful research in transferring mitochondrial genes into the nucleus in cell cultures.
Cell loss and atrophy. Our body's tissues have the means to replace worn-out cells, but this ability is limited in certain organs, says de Grey. For example, the heart is unable to replace cells as quickly as needed as we get older, so it compensates by enlarging surviving cells using fibrous material. Over time, this causes the heart to become less supple and responsive. A primary strategy here is to deploy therapeutic cloning of our own cells, as described on page 22.
Evidence from the genome project indicates that no more than a few hundred genes are involved in the ageing process. By manipulating these genes, radical life extension has already been achieved in simpler animals. For example, by
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