Aurora magazine

Behavioral disorders include a number of attitudes that violate the norms of social life. Children who are affected have a difficult behavior to manage, for parents and educators. Where, however, does the poor education end and the actual disturbance begins?

According to statistics, 6-16% of males under the age of 18 and 2-9% of females suffers from behavioral disorders. The symptoms range from mild to very severe and involve systematic detachment of the child from social norms. Whilst they are scolded and educated, children with these disorders maintain a repetitive and persistent behavior.

The child or teenager suffering from behavioral disorders has manifested at least three of these behaviors over the past 12 months.

• Aggressive behavior. The child looks for physical clash and is cruel with animals and people.
• Vandal acts. The baby does not hurt people but is aggressive with the objects. It damages the properties of others and public ones.
• Thefts and scams. The child mentally systematically does not keep promises and let go of small scams. 
• Violation of legal and moral norms. The child jumps into school and growing alcohol abuse and drugs.

At least one of these must have been evident in the last 6 months, causing discomfort to the subject and others. However, the diagnosis is difficult, as the disorder often occurs along with other problems. Behavioral disorders are associated with 73% of cases of learning disorder and depression. This makes it more difficult to have a clear picture of the situation.

Behavioral disorders often have an environmental source: poor education, difficult family situation, poor socialization. In some cases, however, they are caused by neuropsychological dysfunctions. Many children with early forms of disorder have parents with their own psychopathological disturbances. In these cases, at least one parent suffers from mood disorders and schizophrenia, suggesting a genetic predisposition.

An international study led by Thomas Pizzorusso, a professor at the University of Florence, showed that the eyes affect brain development. The use of vision increases the number of microRNA molecules, which in turn stimulate the development of brain circuits.

MicroRNA molecules regulate how information in genes is transformed into functional macromolecules. Observing the development of the visual bark, the researchers found that it contains a large number of these molecules. In particular, the molecules increase greatly during the functional maturation period in early childhood. According to researchers, microRNA molecules and vision could be linked by virtue of a virulent circle.

The team focused on a particular microRNA molecule, the miR-132. The more miR-132 there are, the greater the functional maturation of vision-related neurons, the excitatory neurons. Without the molecule, development stops and 3D vision is missing. At the same time, visual stimulation induces the production of miR-132. The molecule itself allows proper vision development, which again promotes the rise of miR-132. So brain development stimulates visual development and visual development stimulates brain development.

The discovery opens new perspectives for the study of schizophrenia and autism. In these diseases, gene expression responds abnormally to external experiences. This leads to problems during development. The study identifies some genes controlled by the miR-132 molecule. The cause of some psychiatric illnesses might reside in the way the molecule translates the stimuli.

The molecular factors that mediate stimulation and brain development are relevant even in adulthood. The miR-132 molecule is not present in the brain of patients afflicted with Alzheimer's. This suggests that the absence of a mediator between external and internal world can contribute to brain degeneration.

Source: corriere.it

A Massachusetts General Hospital team (MGH) identified a deficiency in neural stem cells of patients with Huntington's disease. The discovery has allowed us to elaborate a new possible treatment.

The NRF2 transcription factor has the task of protecting cells from external damage. It activates the expression of antioxidant, anti-inflammatory and detoxifying genes. It also acts on all the genes that stimulate the elimination of damaged proteins. Researchers have found that NRF2 is, however, not present in neural stem cells of Huntington's sufferers.

A 2016 study identified a group of components that activates NRF2, called MIND4. MIND4 also inhibits the SIRT2 regulator enzyme, a strategy that has also produced excellent results against Parkinson's. The purpose now is to examine whether MIND4 activates NRF2 only in the guinea pigs or even in humans. If that were the case, it would have a great therapeutic potential.

The researchers also tested MIND4-17, a more powerful version of MIND4. In animal models, the compound increases the expression of antioxidant proteins. It also has the same process that activates NRF2 in response to oxidative stress. In this way, the transcription factor is not degraded by the disease and can activate antioxidant and protective genes.

NRF2 activation also produces anti-inflammatory effects. In particular, it acts on microglia and macrophage cells that penetrate the brain in the last stages of Huntington's disease. This reduces the levels of inflammation and also reduces the effects of the disease.

In Huntington's disease, the HTT gene has a repeated section repeatedly. The human neural stem cells of those suffering from the disease therefore present this problem. The more the repetitions are, the less NRF2 activation affects the symptoms. In cell lines where repetitions were reduced to non-pathological levels, however, activation was more effective. Same thing for non-neuronal cells, on which the effects of the compound were not influenced by the number of repetitions.
Further studies will be needed to test the efficacy of the compound first on animal models, then on the human being. If the tests were successful, there would be a possible treatment for Huntington's disease, Parkinson's and SLA.

Source: medicalxpress.com

Not only acne: a drug used for the skin could also have positive effects against multiple sclerosis. Phase 3 of a clinical trial of the Hotchkiss Brain Institute showed the benefits of minocycline against multiple sclerosis. The discovery offers the possibility for a new "low-cost" treatment against the disease.

One of the main elements of sclerosis is inflammation of the central nervous system, leading to the destruction of myelin. Minocycline is an active ingredient used to treat acne, with many anti-inflammatory properties. Neuroscientist V. Wee Yong then tested minocycline on animal models with the disease. The first tests, dating back to 18 years ago, have been successful.

After success on animal models, the researcher formed his own team and continued with the trials. Today he came to Phase 3, involving 142 patients aged 18 to 60 who had multiple sclerosis. At the beginning of the trial, subjects were passing through the early symptoms of the disease. Each of them received 100 mg of minocycline daily or a placebo. During the 6 months of treatment, there was a 27.6% reduction in disease development.

The results obtained with minocycline are comparable to those obtained with traditional treatments. The main difference lies in the cost. Minocycline is also accessible to lower income bands. This means that you can also take care of those who are economically disadvantaged.

Source: ucalgary.ca