Aurora magazine

The "baby brain" is that set of distractions and omissions that characterize pregnant women. Many future mothers complain, in fact, lack of concentration, difficulty in remembering things and carelessness. Nevertheless, several doctors had relegated the phenomenon to pure exhaustion and suggestion. According to a study by Deakin University, on the other hand, the baby brain exists.

The researchers examined the cognitive functions of 709 pregnant women and 521 non-pregnant women. They submitted the participants to mnemonic and cognitive tests, after which they compared the results. Pregnant women have had worse results than the others, more or less marked depending on the month of gestation. The cognitive decline occurred at the beginning of the first quarter, stabilizing towards the second and until the end of gestation.

The study confirmed that the baby brain is a real phenomenon, but its practical importance is very relative. Pregnant women feel less bright than usual and it's true. However, the phenomenon is destined to disappear after pregnancy, even if the timing is still unclear. More studies will be needed to understand both the reasons for the baby brain and how it takes us to disappear after delivery.

According to a previous study, the baby brain's guilt could be a reorganization of brain functions. The brain would in fact be too busy to process social information useful for raising a child. It would therefore be a natural adaptive phenomenon, necessary to raise the child to the fullest.

Source: ansa.it

Hutchinson-Gilford syndrome or progeria is a fatal genetic disease that causes premature aging. A team led by Dr. Leslie B. Gordon identified a marker protein that could help you choose the best treatments.

Progeria affects about 1 child for every 8 million. Those who suffer seem healthy at birth, but show problems in development within the first year of age. In a previous study, Dr. Gordon's team had tested the effects of the lonafarnib protein, usually used against cancer. Used for 2 years, she helped patients gain weight, reduced the risk of heart attack and the typical headaches of the disease.

Despite the good results of the study, a problem persisted. There were no biomarkers that indicated the effectiveness of the treatment and any problems before they appeared. For this reason, the researchers looked for a marker protein for Hutchinson-Gilford. In this way it would be easier to measure patient progress and understand if there were any changes to be made.

The researchers started from the blood samples of 24 patients between 3 and 12 years. At the time of the study they represented about 10% of the subjects affected by the disease. The samples were taken before and after treatment with lonafarnib and compared with those of some healthy children. Scientists used a tool called RBM HumanMAP to measure levels of about 90 proteins.

The results showed profound different between healthy and sick children in more than 40% of the proteins. All of these could be biomarkers for the disease, to be used for studies and treatments. A big step forward in the fight against this still fatal disease, which could also help in the fight against more common diseases.

Source: springer.com

Researchers at the Huntsman Cancer Institute (HCI) have developed a new way to interpret genetic test results. The merit is also from Bayer's Theorem, a mathematical equation dating back to 1763. The researchers used it as a basis for developing the new evaluation method.

Genetic tests are used in a wide range of areas. They range from fetal DNA tests for prenatal diagnosis to cancer treatments. Test results can help to get more precise diagnoses and develop tailor-made treatments for the individual patient. Depending on what a genetic test says, treatment for the same disease can change significantly.

One of today's big challenges is to understand which genetic variations count and which can be ignored. Over the years, in fact, thousands of VUS have accumulated, or genetic variations whose meaning is unclear. Most of these are almost certainly harmless, but many others could be decisive for the development of a disease.

In order to reduce the subjectivity of certain interpretations, the team developed an algorithm that analyzes the results of genetic tests. The tool serves to determine the risk rate that a patient develops a certain disease. To test its effectiveness, they tested it according to 18 rules recommended by the American College of Genetics and Genomics (ACMG). The results were positive and the new tool proved that it could make the diagnosis more precise.

Source: utah.edu

Multiple sclerosis (MS) is characterized by chronic inflammation of the central nervous system. The immune cells attack the layer of myelin that covers the nerves, making them vulnerable. A study by Professor Mikael Simons of the Technical University of Monaco has unveiled why myelin does not regenerate. Part of the blame would be cholesterol crystals.

Myelin is a membrane enriched with lipids, which isolates nerve fibers. It does so that the electrical signals pass efficiently, getting into the right muscles. When the myelin layer is consumed, the signals disperse and this causes a progressive loss of motor functions. In theory it would be possible to regenerate myelin, but the method proved inadequate in the case of multiple sclerosis.

According to tests by Professor Mikael Simons, part of the blame for non-myelin regeneration would be cholesterol crystals. Myelin contains a lot of cholesterol and releases it all once destroyed. The macrophages take away all the residues they can, but part of the cholesterol accumulates anyway in the cells. In this way, crystals of cholesterol are formed, which cause a persistent inflammation that blocks the regeneration of myelin.

The tests on guinea pigs reveal the importance of age. Depending on the age of the subject, macrophages can eliminate a greater or lesser amount of cholesterol. In older animals, inflammation is stronger and more persistent. Nevertheless, eliminating part of the cholesterol with drugs has in any case helped myelin regeneration.

The discovery is added to some previous studies, which analyzed how myelin developed. Professor Simons and Professor Stadelmann had discovered a new type of cell responsible for the formation of the myelin layer. Applying the new discovery to the previous one opens up new therapeutic possibilities against multiple sclerosis.

Source: medicalxpress.com