The idea of slowing down the ageing process and living healthier, more productive lives is hugely appealing. It’s led to a growing trend for people looking to take control of their own biology, optimising their bodies and minds through ‘biohacking’. But how safe and ethical is this pursuit of longevity? And are there more natural ways of expanding your healthy lifespan? Video by Dan John Animation by Adam Proctor.
Once, at a friend’s wedding, he left a group of guests mildly incensed for suggesting that near-future humans might live well into their 100s. A similar thing happens at dinner parties, where the responses are more polite but no less sceptical. Eventually, he says, “I think we are very likely to have a drug that treats ageing in the next 10 years.” Steele believes we will be hopelessly unlucky if scientists don’t make a breakthrough within that time, given how many human trials are in progress or upcoming. And although these breakthroughs won’t result in treatments that extend our lives by 100 years, they will give us enough extra time to ensure we’re alive for subsequent breakthroughs, subsequent treatments, subsequent additions in lifespan and so on.
The biologist Andrew Steele thinks ageing is a disease that can be treated. But if we had a cure for getting old, what would that mean for us?
Cellular senescence, a state of permanent growth arrest, has emerged as a hallmark and fundamental driver of organismal aging. It is regulated by both genetic and epigenetic factors. Despite a few previously reported aging-associated genes, the identity and roles of additional genes involved in the regulation of human cellular aging remain to be elucidated. Yet, there is a lack of systematic investigation on the intervention of these genes to treat aging and aging-related diseases.
How many aging-promoting genes are there in the human genome? What are the molecular mechanisms by which these genes regulate aging? Can gene therapy alleviate individual aging? Recently, researchers from the Chinese Academy of Sciences have shed new light on the regulation of aging.
Recently, researchers from the Institute of Zoology of the Chinese Academy of Sciences (CAS), Peking University, and Beijing Institute of Genomics of CAS have collaborated to identify new human senescence-promoting genes by using a genome-wide CRISPR/Cas9 screening system and provide a new therapeutic approach for treating aging and aging-related pathologies.
Gene-editing method shows promise for premature aging syndrome.
Scientists have fixed a genetic mutation in mice with progeria, a rapid aging disease. The treatment could one day be used in humans who would otherwise die in childhood.
Approximately 1 in 4 million children are diagnosed with progeria within the first two years of birth, and virtually all of these children develop health issues in childhood and adolescence that are normally associated with old age – including cardiovascular disease (heart attacks and strokes), hair loss, skeletal problems, subcutaneous fat loss and hardened skin.
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▼▼ Description, sources, and more below ▼▼
Two or three meters of DNA are packed into each of your cells, but that careful arrangement gets muddled over time, which is one reason we grow old.
SOURCES AND FURTHER READING
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Larson K, Yan SJ, Tsurumi A, Liu J, Zhou J, Gaur K, Guo D, Eickbush TH, Li WX. (2012) Heterochromatin formation promotes longevity and represses ribosomal RNA synthesis. PLoS Genet. 8:e1002473.
Oberdoerffer P, Sinclair DA. (2007) The role of nuclear architecture in genomic instability and ageing. Nat Rev Mol Cell Biol. 8:692–702.
Pegoraro G, Kubben N, Wickert U, Gohler H, Hoffmann K, Misteli T. (2009) Ageing-related chromatin defects through loss of the NURD complex. Nat Cell Biol. 11:1261–1267.
Pollina EA, Brunet A. (2011) Epigenetic regulation of aging stem cells. Oncogene 30:3105–3126.
Andrew Steele is a scientist, writer and presenter.
Ageing is a phenomenon we’re all familiar with and is completely taken for granted as a fact of reality, but do we have to accept.
Expect to learn why curing ageing might be easier than curing cancer and all other diseases, the unfortunate truth of fasting for longevity, why the next decade will be the most exciting for lifespan research and much more…
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One mouse is hunched over, graying, and barely moves at 7 months old. Others, at 11 months, have sleek black coats and run around. The videos and other results from a new study have inspired hope for treating children born with progeria, a rare, fatal, genetic disease that causes symptoms much like early aging. In mice with a progeria-causing mutation, a cousin of the celebrated genome editor known as CRISPR corrected the DNA mistake, preventing the heart damage typical of the disease, a research team reports today in. Treated mice lived about 500 days, more than twice as long as untreated animals.
“The outcome is incredible,” says gene-therapy researcher Guangping Gao of the University of Massachusetts, who was not involved with the study.
Although the developers of the progeria therapy aim to improve it, they are also taking steps toward testing the current version in affected children, and some other scientists endorse a rush. The mouse results are “beyond anyone’s wildest expectations,” says Fyodor Urnov, a gene-editing researcher at the University of California, Berkeley. “The new data are an imperative to treat a child with progeria … and do so in the next 3 years.”
Has some interesting parts, might interest some.
(not sure how novel)
As human beings age, the functioning of organs gradually deteriorates. While countless past studies have investigated the effects of aging on the human body, brain and on cognition, the neural mechanisms and environmental factors that can accelerate or slow down these effects are not yet fully understood.
The immune system and the nervous system are both known to play a key role in the control of organs in the body. Moreover, past findings suggest that both of these systems change significantly during aging.
Neuroscientific studies have found that as the nervous system ages, the way in which the human body controls immune responses also changes. Nonetheless, how the nervous system’s aging process affects immune responses and the consequent impact on the brain’s functioning are still poorly understood.
After the tweet by David Sinclair just recently regarding a study looking at dietary restriction and the circadian clock, and the way it may impact longevity and health, I decided to have a bit of a deeper look.
Join me as I dive a little deeper, and don’t forget to subscribe to the channel to keep up with all the latest releases.
I am looking at the recent study, highlighted in a tweet by David Sinclair.
This study, although only in fruit flies, shows interesting linkages between food intake, the circadian clock and longevity.
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Why not check out this video next on sleep deprivation :
The study can be examined in detail here:
https://www.biorxiv.org/content/10.1101/2020.09.14.296368v2.full.
The theory of the disposable soma referenced :
http://www.programmed-aging.org/theories/disposable_soma.html.
The theory of the bloated soma referenced :
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5395017/
Summary: People with spinal cord injuries have the same brain activity during processing speed tasks as healthy older adults. The findings suggest the theory of accelerated cognitive aging following SCI is correct.
Source: Kessler Foundation.
A team of rehabilitation researchers has studied processing speed deficits in individuals with spinal cord injury (SCI), comparing their brain activation patterns with those of healthy age-matched controls, and older healthy individuals. They found that the SCI group and older controls had similar activation patterns, but the SCI group differed significantly from their age-matched controls.
