Thursday, September 21

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Scientists finally discover why we grow old and die!

by Staff writer



One of the biggest questions thrown at science is why we age and die...

Why we didn't evolve to live forever...

Researchers at the Institute of Molecular Biology (IMB) in Mainz, Germany, have made a breakthrough in understanding the origin of the ageing process.


They have identified that the same genes involved in a process called autophagy drive the process of ageing later in life.

One of the cells' most critical survival processes, autophagy describes a process where cells create membranes that hunt out scraps of dead, diseased, or worn-out parts and then gobble them up, using the resulting molecules for energy or to make new cell parts.

This powerful natural recycling ability of our cells has been credited as making us more efficient machines by getting rid of faulty parts, stopping cancerous growths and metabolic dysfunction like obesity and diabetes.

According to the research paper, while autophagy promotes health and fitness in young worms, it appears to completely deteriorate in older worms.

The research authors were able to demonstrate that shutting down key genes in the initiation of the process allows the experimental worms to live longer compared to those in the control group.

The research published in the journal Genes and Development gives some of the first clear evidence for how the ageing process arises as a quirk of evolution.

These findings may also have broader implications for the treatment of neurodegenerative disorders such as Alzheimer's, Parkinson's, and Huntington's disease where autophagy is implicated.

The researchers show that by promoting longevity through shutting down autophagy in old worms there is a strong improvement in neuronal and subsequent whole body health.

Getting old is something that happens to everyone and nearly every species on this planet, but the question is, should it?

"The evolutionary theory of ageing just explains everything so nicely but it lacked real evidence that it was happening in nature," explained co-lead author of the paper Jonathan Byrne.

"Evolution becomes blind to the effects of mutations that promote ageing as long as those effects only kick in after reproduction has started. Really, ageing is an evolutionary oversight." Jonathan continues.

"These AP genes haven't been found before because it's incredibly difficult to work with already old animals, we were the first to figure out how to do this on a large scale."

He explains further "From a relatively small screen, we found a surprisingly large number of genes [30] that seem to operate in an antagonistic fashion."

Previous studies had found genes that encourage ageing while still being essential for development, but these 30 genes represent some of the first found promoting ageing specifically only in old worms.


"Considering we tested only 0.05% of all the genes in a worm this suggests there could be many more of these genes out there to find," says Jonathan.

By inactivating autophagy in the neurons of old worms the researchers were not only able to prolong the worms' life but they increased the total health of the worms dramatically.


"Imagine reaching the halfway point in your life and getting a drug that leaves you as fit and mobile as someone half your age who you then live longer than, that's what it's like for the worms," says Thomas Wilhelm, the other co-lead author on the paper.

"We turn autophagy off only in one tissue and the whole animal gets a boost. The neurons are much healthier in the treated worms and we think this is what keeps the muscles and the rest of the body in good shape. The net result is a 50% extension of life."

While the authors do not yet know the exact mechanism causing the neurons to stay healthier for longer, this finding could have real world implications.

"There are many neuronal diseases associated with dysfunctional autophagy such as Alzheimer's, Parkinson's, and Huntington's disease, it is possible that these autophagy genes could represent a good way to help preserve neuronal integrity in these cases," elaborates Thomas Wilhelm.

While any such a treatment would be a long way off, assuming such findings could be recapitulated in humans, it does offer a tantalizing hope; prevent disease and help people live longer and healthier lives.

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