For the first time a gene was identified that allows the repair of damaged nerves in nematodes. The study is from Science Express. A gene that can stimulate the growth of nerve cells was first identified by researchers at the University of Utah (USA), thanks to cutting-edge experimental techniques and a huge genetic screening on a nematode (cylindrical or worm). The neurons, which in the embrio are able to regenerate, in adults have their capacity to "repair" reduced or absent. In other words, damage to the central nervous system (brain or spinal cord) and its consequences - paralysis, loss or reduction of cognitive faculties - are permanent. "In the past molecules have been identified that can inhibit the growth of neurons in different organisms," says the coordinator of research Michael Bastiani, "but their removal in the laboratory had no effect. That is why we went to look for those genes that can stimulate rather than inhibit, the regeneration of nerve. " Taking as a experimental model flat worms (Caenorhabditis elegans), biologists have searched for the genes that trigger the regrowth of motor (neurons that "command" voluntary muscles): in practice, with an experimental technique called RNA interference to "shut down ", one by one, 5000 on 20,000 genes in the DNA of worms (genes similar are also present in humans). The analysis led to the identification of dlk-1, which appears to play a key role in the regeneration of nerve tissue, and three other genes responsible for the formation of axons (parts of the neuron that conduct electrical signal). The researchers found that in nematodes, the gene dlk-1 not only triggers a chain of events known as "Map kinase" behind the growth of neurons, but also that their regeneration can be increased or decreased by stimulating the gene to produce amounts more or less high of the protein dlk-1.

Npas4: This protein regulates the formation of inhibitory synapses between neurons. The inhibitory activity of neurons is regulated by a particular switch. This is a protein involved in the formation and maintenance of synapses in regulating selectively switching the electrical signal between nerve cells. Its name is Npas4 and was discovered by researchers from the Children's Hospital in Boston this week to publish their study in Nature. In particular, the protein in question is a transcription factor, that is a molecule that can activate or deactivate specific genes. Those which would be linked to Npas4 are more than 270. When the protein is produced in large quantities, we are seeing an increase in the number of inhibitory synapses on the surface of nerve cells. But what induces the production of high levels of Npas4? According to the researchers this is a reaction to excitatory synaptic. "It is as if the same excitement triggers a program to rebalance the brain with inhibition," says Michael Greenberg, coordinator of the study, which continues: "The mice in which the protein is suppressed, in fact, have neurological problems: are anxious, hyperactive and more subject to seizures. " The discovery could help researchers in studying these disorders. Inhibition, in fact, plays an important role in brain development.

The ventral striatum, a part of the brain already known to be associated with rewards and unexpected stimuli, is the center of our desire for adventure. The research in Neuron. A group of researchers from the Wellcome Trust Centre for Neuroimaging at the University College of London has identified the area of the brain directly linked to our desire for adventure. Or, more precisely, our propensity to live new experiences and to experience what we do not know. For the study, published in Neuron, researchers have developed a test: the participants were presented a series of images associated with different sums of money put into a premium, and were asked to guess which of the sums was higher. Although the volunteers easily could identify the image associated with richer rewards, when it was introduced a new figure, all of them tended to choose the latter rather than those already known with secure profits. Through magnetic resonance imaging, neuroscientists have noticed that the area of the ventral Striatum (an area of the brain already known to be associated to receive a reward and unexpected stimuli) was particularly active when participants opted for the novelty.

A newly discovered molecule, Isx-9, is able to make stem cells mature into brain cells. The study in Nature Chemical Biology They came across this behavior, while they were stimulating stem cells to give rise to cardiac cells, when researchers from the Southwestern Medical Center at the University of Texas at Dallas, have discovered that some of the molecules tested have matured however into neural cells. Completely random, therefore, this lead to the isolation of Isx-9, the most powerful among the compounds tested, capable, at very low concentrations, to create differentiated neurons. The study, conducted by researchers led by Jay Schneider and Jenny Hsieh was published on the number of Nature Chemical Biology. Scientists began testing 147 thousand molecules for the project in order to isolate those who could stimulate embryonic stem cells to differentiate into cardiac cells. Stunningly, American researchers have noted that five of these compounds caused the stem to rise to neurons. One of these molecules was selected because it was acting to lower concentrations of the other and was more soluble in water. This, has given life to the compound Isx-9 that has been tested on neural stem cells from the brain, particularly those of the hippo campus of laboratory animals. In the test tube, the stem, under the action of Isx-9, could form the clusters and develop the first steps towards the formation of neurons.

An Italian research published on Plos One identified, in rabbits, some areas where neurons grow as from adult tissue A new Italian study has identified in the cerebellum of rabbits some areas in which nerve cells grow from adult tissue, demonstrating that repairing damaged to the brain - in theory - is not impossible. The discovery, fifteen years ago, that even the central nervous system of adult mammals can form new neurons has been a cornerstone of neuroscience and distorting the previous belief that neurogenesis occurs in this animal class, once and for all, during development embryonic, without the possibility of repair after birth. Unlike other vertebrates, in which this process occurs post-natal widely in the brain, in mammals seems limited to a few specific areas.

In these monkeys 80 per cent of the neuron cell cortex is multisensory phonetic and also responds to visual stimuli. Thus, all the information is integrated It is known for some time that monkeys are able to integrate information in various ways to recognize monkeys in the group and their intentions, just like us and like many other other animals. What we did not know until today was how our "cousins" could associate verses and faces, optimising thus the process of individual recognition. The experiment helps to clarify that which was published in Journal of Neuroscience and was conducted by Aif Ghazanfar and collaborators at Princeton (USA) on a kind of macaco. The researchers found that, in these monkeys, many neurons are in fact multi-sensorial and respond differently depending on whether the hearing and visual stimuli are at the same time or not. For monkeys, which live in social groups and must manage complex relationships - conflicting and friendly - it is crucial to combine auditory stimuli (leading information-type sound, as a sound threat) and images (which provide summary information, such as the color of skin or facial features). The group Ghazanfar could shed light on the mechanism of integration of different stimuli by measuring the activity of visual and auditory cortex areas of the brain, respectively, for image and sound. Measurements were made under different conditions: in one case the animals could both see fellow companions in the group, listen to their sounds, while in other cases the animals could alternatively listen to the auditory component only or see the companions (only visual component).

Cloned cells were transplanted into the brain of mice who suffered from this disease and they replaced sick neurons. The success of therapeutic cloning in mice. Researchers of the Sloan-Kettering Institute in New York, led by neuro-scientist Lorenz Studer, have treated the guinea pigs suffering from Parkinson with the transplantation of embryonic stem cells obtained from the skin of rodents themselves sick. The experiment, described in Nature Medicine, not only has recorded cases of rejection, but also significant improvements in the evolution of clinical pathology. The group Studer - after having caused lesions in the brains of mice that would determine the same effects of Parkinson's disease - has transferred the nuclei of cells inside the tail skin cell mouse egg "emptied" of its nucleus, through the technique known as therapeutic cloning (or Scnt, Somatic Cell Nuclear Transfer). The cloned cells, cultivated, were then developed into blastocysts. The researchers thus generated 187 lines of embryonic stem cells from 24 different mice, most of which later differentiate into neurons capable of producing dopamine.

Using functional magnetic resonance imaging, researchers have been able to associate a brain activation pattern to the memory of an image. According to a study in Nature. Reading the thoughts of other people is not yet possible, but scientists are working on it. One tool developed by Jack L. Gallant and collaborators at the University of Berkeley (California) is able to recognize an image that a person has just seen through his brain activity. Two of the authors of the study published in Nature - Kendrick Kay and Thomas Naselaris - were submitted in person by observing the experiment at random photographs from a group of 120 during brain scans using functional magnetic resonance (fMri). The results of fMri, combined with a mathematical model, have served to associate the images neuronal activity that a person has just had before our eyes.

Even a visual stimulus extremely short, less than millisecond, affects the decoding of information in the nervous system. The Ferrari of insects, the horsefly, a tiny acrobat who moves at high speed, has proved that even a very short visual stimulus (on the scale of milliseconds) affects decoding information in the nervous system. This was discovered by scientists in universities of Indiana, Princeton (New Jersey) and the Los Alamos National Laboratory (New Mexico), one of the largest multidisciplinary institutions in the world. A human being is unable to record the continuous change of scenery and should have a supra-sensory stimulation. But this is a fly: its nervous system processes information very quickly so that the insect can adapt to what he sees with a reaction time of 30 milliseconds. "During the flight," says Ruyter van Steveninck University of Indiana, "the horsefly must quickly analyze a number of complex information and, because of its ability to move rapidly, it is reasonable to think that the way it deciphers level sensory-motor data is optimal. We then decided to study its visual system to understand how his brain can order a continuous stream of very complex data in such an efficient way. "

The procedural memory remains imprinted in the chemical synapses. It is not the merit of a cell constant. When we drive a car or we tie a shoe knot, we store a series of gestures that are accessed faster and automatically whenever you need that action again. It is the so-called working memory or procedural memory, whose operation resembles that of cache memory of a computer, for example, allows us to more quickly open a website already visited. A study conducted by Gianluigi Mongillo of French Cnrs research, and Omri Barak and Misha Tsodyks the Weizmann Institute (Israel) would seem to refute the widespread belief that this type of memory is fixed thanks to a number of specific neurons. On the contrary, the procedural memory is recorded at the level of chemical changes in cells that remain after the transition pressure in nervous synapses (points of contact and communication between neurons).

Muliple mutations of a single gene lead to the accumulation of a protein in motor neurons that causes death. Mutations in a single gene could be the basis of amyotrophic lateral sclerosis (Sla), the neurodegenerative disease that leads to progressive paralysis and that affects every year in Italy 1,500 people, mainly men of average or advanced age. The discovery, the result of years of studies conducted by international team in which the names of Emanuele Buratti Baralle Francisco and the International Centre for Genetic Engineering and Biotechnology (Icgeb) in Trieste, and guided by Christopher Shaw of King College London, appeared in Science.