S ay this about the types of molecular chaos that we know they underlie aging: mechanisms such as whether the ends of chromosomes are fraying (bad) and whether the on-off status of genes at least bad (really bad) sounds plausible ways to affect vital organs, from the skin over the brain to the heart, and to cause the well-known as aging, sad mess.
On Wednesday, scientists reported a driver of aging that even the senior researcher diplomatically calls "counterproductive." : neural activity. Of course, aging affects the brain. But the brain also seems to affect aging, they found out: In living things, from worms to mice to humans, high levels of neuronal firing mean a shorter lifespan. Lower levels ̵
The discovery was so surprising that it took two years for it to be published (in Nature), as the external scientists requested the study to be assessed with additional data. Geneticist Bruce Yankner of Harvard Medical School, who led the research, understood her skepticism. "If you say you have a cat in your backyard, people will believe you," he said. "If you say you have a zebra, you want more evidence."
Evidence is what he and his colleagues have produced in humans and mice and the roundworm C. elegans, which has been around for a long time is common in biology. "I think this is a significant new discovery," said molecular biologist Nektarios Tavernarakis of the University of Crete, an aging expert who has reviewed the paper for nature. "It's definitely a surprising turn in the saga of aging, but it's still too early to talk about manipulating the human lifespan on that basis." In my opinion, things get more complicated. On the other hand, previous studies have suggested that excessive neural activity is a factor for dementia, and some Alzheimer's experts recommend yoga and meditation (both of which can alleviate the disease) brain) as possible ways to slow the progression of this life-shortening disease to slow down. Given the additional evidence linking life-span neuronal activity, the notion that neuron-calming medicines might someday prolong life span seems a little less far-fetched.
Along Nerve Cells – this may have something to do with the lifespan that comes from human brains donated for research purposes. In the frontal cortex, the place of higher order thinking, a gene called REST was more active in the brains of people over 85 years old than in the frontal cortex of brains whose owners died in the sixties or seventies. (The detection of gene activity lasts for months in dead brains when properly frozen.) All brains were cognitively normal.
REST did not come by accident. In 2014, Yankner and his colleagues showed that this gene protects the aging brain from dementia.
"REST is involved in neuronal arousal and is normally active during development of the fetal brain," Yankner said. "After that, it's usually turned off. But as the brain ages, it seems to turn back on "- more in some people than others. REST, whom Yankner calls "a master of gene regulation" that relieves neuronal activity, "occurs in people who live longer," he said.
That does not seem intuitive. "One would expect more neuronal activity to be associated with a longer life," Yankner said. However, the lower activity in the world's Methuselahs is not so low as to affect thought – it's just so quiet that your brain uses no more energy for a problem than, say, people decades younger. On average, imaging studies show that older people have more intense and comprehensive brain activity when they think about a mental health problem, while young brains and middle-aged brains are more neuronal-efficient. It's like the difference between a champion runner's wasted movement and the bouncing arms and legs of a weekend jogger.
The association between the low level of neuronal activity of the human brain due to a high REST level On the other hand, a longer lifetime could be more of a coincidence than cause and effect. To find out if neuronal activity affects life expectancy, scientists inhibited this activity in C. elegans by also increasing activity in the worm version of the neuron-calming REST gene.
The worms live around you with shocked neurons. Third longer – four weeks instead of the usual three. The Harvard scientists performed similar experiments on mice and found the same. "The animals could still work – we did not hibernate their brains," Yankner said. "But by suppressing neuronal activity, you can influence the aging process."
Together, the experiments with mice and worms are strong evidence that milder neurons prolong lifespan. "I think they've found that neuronal activity is a determinant of longevity," said Tavernarakis.
It is not clear how exactly quieter neurons extend the life span. One note: It is known that lowering neuronal activity activates genes that protect the brain (and the body) from stress. The same resilience genes are also activated by calorie restriction, which similarly prolongs the life of worms and mice.
This makes REST and other molecules that control neuronal excitability a possible target for intervention to combat age decline and disease, "wrote Tavernarakis in an article in Nature.
Yankner and his colleagues were not exactly sitting around and doing nothing in the two years since they submitted their study to Nature. They have investigated compounds that could increase the activity of the REST gene in order to calm neuronal activity and extend the life expectancy of humans. However, it is far too early to determine if any of these potential medicines are safe or even effective.