The life span of nematodes has been prolonged by 500% with new genetic manipulations

A new cell pathway that amplifies the lifespan of Caenorhabditis elegans, an approximately one-millimeter long nematode that usually lives in soil, has been identified by a team of researchers at the Buck Institute for Research on Aging in Novato, California and the University of Nanjing, China.

Specifically, this new cell pathway can extend the life of this small worm, which usually lives up to 3-4 weeks, by five times: if the thing could be applied, for example, even to a human being, it could extend the life of the latter up to a duration of 400 or even 500 years.

Of course, we are very far from a possible application on humans due to the extreme complexity of our body and our genetic profile compared to that of a nematode, however thanks to the fact that this nematode shares with us many of its genes, the result is certainly worthy of note in the context of the fight against aging. Specifically, researchers have genetically altered the insulin signalling pathways (IIS) and the target of the rapamycin pathway (TOR), as well as other mitochondrial functions.

These are genetic manipulations that, at least on this worm, have led to an almost exponential effect, as Jianfeng Lan, a researcher who participated in the study, suggests: “The effect is not one plus one equal to two, it is one plus one equal to five. Our results show that nothing exists in nature in a vacuum; in order to develop the most effective anti-aging treatments we must look rather at the longevity networks of individual pathways.”

Now researchers want to understand more about the actual role of the mitochondria of aging probably also to understand if any genetic manipulation could have a similar effect on humans.

Losing even one night’s sleep increases Tau protein in the brain, an Alzheimer’s marker

Losing even one night’s sleep increases levels of Tau, abundant proteins in central nervous system neurons that can be considered a marker of senile dementia, particularly Alzheimer’s disease.
This is the discovery made by a team of researchers at the University of Uppsala who published their study on Neurology.

Tau proteins present in neurons usually form “tangles.” When the formation of these tangles exceeds a certain limit, they accumulate in the brain and lead to Alzheimer’s disease. Before the symptoms of the same disease appear, the accumulation can last for decades. Already in the past, studies had shown that Tau levels in cerebral spinal fluid could increase as a result of sleep deprivation.

According to Jonathan Cedernaes, one of the authors of the study, even a single night’s sleep can cause an increase, albeit slight, in the level of tau in the blood. This, in turn, suggests that repeated sleep interruptions or long-term sleep deprivation can therefore have harmful effects in terms of cognitive function and the risk of Alzheimer’s itself.

The researchers carried out studies on 15 healthy men with an average age of 22 years who had reported, before the start of the experiment, to sleep regularly from seven to nine hours a night.
In the first phase, these people observed a rigorous program of meals and physical activity for two days two nights. After this first phase, blood samples were taken and analyzed.

Then the second phase began, during which the same people were given a normal night’s sleep, followed by a night in which they were kept forcibly awake with lights on and various activities. Subsequent blood tests showed a 17% increase in blood tau levels after just one night of sleep deprivation. The researchers also examined four other Alzheimer’s related biomarkers but these were not characterized by any particular changes or increases.

According to Cedernaes himself, this is explained by the fact that when neurons are active, the release of TAU in the brain is higher than when we sleep. That is why after only one night when awake, the amount is increased the next day.

Now further studies are needed to determine whether these increases cause a general increase in tau levels in the brain over the long term or whether these proteins are eliminated in whole or in part somehow after a sleepless night. Further studies should also be carried out on different populations, e.g. female patients or elderly people.