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.

A new instrument will allow mass measurement of exoplanets with extreme precision

A new instrument just mounted on the 3.5-meter WIYN telescope at Kitt Peak National Observatory in southern Arizona promises to detect mass and other characteristics of exoplanets with unprecedented accuracy. In fact, the new instrument, called NEID, will allow an accuracy three times higher than the previous generation of similar instruments.

A high-precision radial velocity spectrometer will collect light from the stars and measure the sometimes minimal gravitational effect that the planets themselves have on the stars around which they orbit. It is a small “wobble” caused by a periodic shift in the speed of the star. This also happens in our solar system. For example, Jupiter, the largest planet, causes an oscillatory movement of the Sun that can be measured in about 30 miles per hour. The Earth, on the other hand, causes a movement of only 0.2 miles per hour.

Of course, the size of the oscillation is proportional to the mass of the planet and this is why it is possible not only to discover the planets themselves but also to measure their mass with extreme precision. The similar instruments used until now can in fact measure this type of oscillation only up to 2 miles per hour but now the NEID will be able to measure oscillations at even shorter speeds, up to one mile per hour, as explained by Jason Wright, a researcher at the State University of Pennsylvania involved in the project. This means that even exoplanets with a land mass can be more easily discovered.

Such an instrument, in collaboration with others such as the TESS space telescope, will therefore allow a greater number of discoveries of exoplanets so that “things will become really interesting and we will be able to learn what planets are made of,” as the scientist himself explains.

The instrument has already been tested with observations of the brightness of the star 51 Pegasi. The instrument can also be updated and can be used by practically all astronomers, as explained by Sarah Logsdon, another researcher involved in the project.

Supplements with zinc and folic acid do not improve male fertility according to a new study

Supplements based on zinc and folic acid, increasingly propagated as substances to combat male infertility, are not actually responsible for an improvement in pregnancy rates, sperm count and potency. This is the conclusion in a statement published on the University of Utah’s website which refers to a new study published in JAMA.

According to the researchers, this is the most definitive proof obtained to date through a scientific study of the fact that these supplements do not actually meet expectations. “The message for men to take home is that, for the first time, there is high-quality data that zinc and folic acid do not improve live birth outcomes or semen function,” says James M. Hotaling, a urologist at the university and one of the authors of the study.

Among the most popular fertility supplements are those containing zinc, which is actually essential for sperm development. These supplements very often also contain folic acid, another substance that actually helps the DNA formation process of the spermatozoa themselves. However, over-the-counter supplements, also called nutraceuticals, containing these substances do not seem to produce a satisfactory result.

This is the result that the researchers obtained by performing an experiment on 2370 couples who had planned to undergo fertility treatments in various U.S. cities. Some of the men were given a supplement consisting of 5 mg of folic acid and 30 mg of zinc for six months. The remaining men were given a placebo substance.

At the end of the experiment, the researchers found no particular differences in the number of live births between men who had taken the supplement and those who had not. The group of the placebo substance showed 35% of live births compared to 34% of the first group.

In addition, the subjects in the group that had received the supplement, compared to the placebo group, had complained more abdominal pain, vomiting, nausea and other gastrointestinal symptoms.

Deaf people have “rewired” brains that influence learning according to a new study

According to a new study published in Nature Scientific Reports, the brains of people with congenital deafness can develop differently and this can influence the ways in which these same people learn to learn. This study, according to the same researchers, may prove useful precisely to develop new methods of teaching “tailor-made” for all people who have never had the opportunity to use hearing during their existence.

According to Colin Johnson, a researcher at the College of Science of the State University of Oregon, people who are born deaf can have a life that is severely compromised even with regards to school and teaching in general. Often these people, in fact, as specified by the researcher, generally fail to reach an adequate level of education and this leads to cascade to other consequences that certainly do not improve the standard of living.

Researchers have discovered that it is a particular protein mutation that causes hearing loss and that it can also alter the wiring of different groups of neurons. The protein, known as otoferlina, has the sole task of encoding the sound in the sensory hair cells that are found in the inner ear.

If this protein undergoes a genetic modification, total hearing loss can occur. This mutation weakens the link between the protein and a calcium synapse in the ear and this lack of interaction is the basis of hearing loss.

Studying this protein in humans has always been difficult due to its size and due to the fact that it is characterized by low solubility. That is why Johnson and colleagues have studied zebrafish that share a similarity in genetic, molecular and cellular levels with humans.

Thanks to these studies, the researcher has discovered a smaller version of the otoferlina that could be used for gene therapy but only in those brains that have not yet undergone a complete rewiring such as that of adults.

“If you grow up without that protein, it’s not just a matter of replacing the gene. If you are deaf and grow deaf, it seems that the physical wiring of your brain is a little different. This complicates the goal of doing gene therapy. We need to go further and look at these hair cells and the brain itself. Does the brain process information differently? This is an area we need to focus on,” explains Johnson.

Ghrelin can increase the urge to exercise according to a new discovery

As some researchers have observed when performing experiments on mice, limiting access to food can increase the levels of a particular hormone, called ghrelin, and this in turn can increase the motivation to exercise, something that naturally leads, in a chain effect, slimming.

In the study, published in the Journal of Endocrinology, it is described how the increase in the level of this hormone pushed mice to voluntarily start exercising or physical activity. This finding, according to the same researchers, could lead, through the limitation of food intake or through the so-called “intermittent fasting,” overweight people to be encouraged to exercise more.

On the other hand, the restriction of food the same regular exercise are the two main ways and the most economic strategies to prevent and treat obesity, a sort of global “epidemic” that requires much more effective intervention strategies. However, adhering to a regular training regime can be difficult for many because motivation is lacking.

This hormone, also called the “hunger hormone,” can not only stimulate the appetite but, as demonstrated by Yuji Tajiri and colleagues from the Kurume University medical school, Japan, it can also stimulate the same desire to exercise. The mice genetically modified in the laboratory for not having ghrelin of their body, in fact, ran less than the control mice, which instead had normal ghrelin levels.

According to Tajiri, the results achieved by this study indicate “that hunger, which promotes ghrelin production, could also be involved in increasing motivation to voluntary exercise when nutrition is limited. Therefore, maintaining a healthy diet, with regular meals or fasting, could also encourage motivation for exercising in overweight people.”

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