that human diseases should have been eradicated by
natural selection by now via inherited immunity or random mutation. The reason they haven’t been is therefore because humans mate young, and for most of our evolution have also died young. The presence of extensive age-related disease is a relatively new phenomenon because it’s only recently that people have reached their seventies and beyond on a regular basis. This
means that natural selection only acts weakly against age-related disease because resilience to it hasn’t yet had the chance to evolve within us. My work involved studying how genetic
manipulation might serve humanity by acting as a substitute for natural selection and creating specific genes resistant to such diseases, like Huntingdon’s or Alzheimer’s.’
‘Okay,’ Lopez said, ‘so how would you go about doing that?’
‘Well,’ Willis replied, ‘the main cause of aging in mammals is the degradation of telomeres in the nuclei of cells. Telomeres are like caps at the tips of chromosomes –
you can think of them as fuel for the accurate division and replication of cells. As cells divide, telomeres become ever shorter, and eventually they are unable to support further cellular division
without a build-up of errors or deleterious mutations, which cause the signs of aging such as muscle loss, degraded skin quality, organ failure and so on. If we can find a way of allowing cells to
divide without losing the telomeres and building up those errors, we have a possible means of extending quality of life, if not longevity itself.’
‘Doesn’t sound so hard,’ Ethan said.
‘It’s hard,’ Willis assured him. ‘Mainly because the only kind of cells that naturally undergo this transformation into biologically immortal cells are those that cause
cancer. The line between the two may be thin, but it’s the difference between curing someone and killing them.’
‘And you’ve figured out a way to do this?’ Lopez asked.
‘There are a number of potential ways,’ Willis replied, ‘to slow aging in mammals. Cell loss can be repaired via growth factors to stimulate cell division, such as stem cells,
or even by simple methods such as exercise or reduced calorie intake. Senescent cells can be removed by activating the immune system against them or via gene therapy. Extracellular materials like
amyloid can be eliminated by vaccination, while intracellular junk requires the introduction of new enzymes that can degrade the junk that our own natural enzymes cannot degrade. Mitochondrial
mutations can be handled using gene therapy via cell nuclei. For cancer the strategy is to use gene therapy to delete the genes for telomerase and to eliminate telomerase-independent mechanisms of
turning normal cells into ‘‘immortal’’ cancer cells. To compensate for the loss of telomerase in stem cells we would introduce new stem cells every decade or so.’
‘Has any of this actually been achieved?’ Ethan asked.
‘The Dana-Faber Cancer Institute managed to reverse the aging process in mice,’ Willis said, ‘by targeting the chromosomes in cellular nuclei and the telomeres. They
manipulated the enzyme that regulates these tips, telomerase, turning it on and off. When they boosted the enzyme, the mice appeared rejuvenated. There was a dramatic reversal in the signs and
symptoms of aging: the brains increased in size, cognition improved, coat hair regained a healthy sheen and fertility was restored. It was the equivalent of taking someone from their eightieth year
and bringing them back to their forties. They had in effect undergone rejuvenation, had become young again.’
‘Holy crap,’ Lopez smiled. ‘That could be worth a fortune!’
‘It was only in mice,’ Willis cautioned, ‘and there’s a lot of work to be done, mostly in figuring out how to make elderly people more comfortable and to remove the
specter of age-related disease. That said, there are people looking to make money
natural selection by now via inherited immunity or random mutation. The reason they haven’t been is therefore because humans mate young, and for most of our evolution have also died young. The presence of extensive age-related disease is a relatively new phenomenon because it’s only recently that people have reached their seventies and beyond on a regular basis. This
means that natural selection only acts weakly against age-related disease because resilience to it hasn’t yet had the chance to evolve within us. My work involved studying how genetic
manipulation might serve humanity by acting as a substitute for natural selection and creating specific genes resistant to such diseases, like Huntingdon’s or Alzheimer’s.’
‘Okay,’ Lopez said, ‘so how would you go about doing that?’
‘Well,’ Willis replied, ‘the main cause of aging in mammals is the degradation of telomeres in the nuclei of cells. Telomeres are like caps at the tips of chromosomes –
you can think of them as fuel for the accurate division and replication of cells. As cells divide, telomeres become ever shorter, and eventually they are unable to support further cellular division
without a build-up of errors or deleterious mutations, which cause the signs of aging such as muscle loss, degraded skin quality, organ failure and so on. If we can find a way of allowing cells to
divide without losing the telomeres and building up those errors, we have a possible means of extending quality of life, if not longevity itself.’
‘Doesn’t sound so hard,’ Ethan said.
‘It’s hard,’ Willis assured him. ‘Mainly because the only kind of cells that naturally undergo this transformation into biologically immortal cells are those that cause
cancer. The line between the two may be thin, but it’s the difference between curing someone and killing them.’
‘And you’ve figured out a way to do this?’ Lopez asked.
‘There are a number of potential ways,’ Willis replied, ‘to slow aging in mammals. Cell loss can be repaired via growth factors to stimulate cell division, such as stem cells,
or even by simple methods such as exercise or reduced calorie intake. Senescent cells can be removed by activating the immune system against them or via gene therapy. Extracellular materials like
amyloid can be eliminated by vaccination, while intracellular junk requires the introduction of new enzymes that can degrade the junk that our own natural enzymes cannot degrade. Mitochondrial
mutations can be handled using gene therapy via cell nuclei. For cancer the strategy is to use gene therapy to delete the genes for telomerase and to eliminate telomerase-independent mechanisms of
turning normal cells into ‘‘immortal’’ cancer cells. To compensate for the loss of telomerase in stem cells we would introduce new stem cells every decade or so.’
‘Has any of this actually been achieved?’ Ethan asked.
‘The Dana-Faber Cancer Institute managed to reverse the aging process in mice,’ Willis said, ‘by targeting the chromosomes in cellular nuclei and the telomeres. They
manipulated the enzyme that regulates these tips, telomerase, turning it on and off. When they boosted the enzyme, the mice appeared rejuvenated. There was a dramatic reversal in the signs and
symptoms of aging: the brains increased in size, cognition improved, coat hair regained a healthy sheen and fertility was restored. It was the equivalent of taking someone from their eightieth year
and bringing them back to their forties. They had in effect undergone rejuvenation, had become young again.’
‘Holy crap,’ Lopez smiled. ‘That could be worth a fortune!’
‘It was only in mice,’ Willis cautioned, ‘and there’s a lot of work to be done, mostly in figuring out how to make elderly people more comfortable and to remove the
specter of age-related disease. That said, there are people looking to make money
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