Researchers approach the interpretation of the complex nature of unknown autism

A team of researchers revealed a molecular mechanism that explains how changes in (CPEB4 protein) can contribute to unknown autism, a type not related to a well -known genetic boom, according to a study they published in the journal Nature. Ciceb4 protein belongs to the protein family associated with regulating the translation of RNA, and plays an important role in controlling genetic expression within the cells. The research team of the Spanish Biomedical Research Institute focused on a small part of the protein known as “neuronal microxons”, which was essential for nerve growth. CPEB4 protein is a key to regulating nerve proteins for autism. In a previous study in 2018, the researchers discovered that individuals with autism do not have a small part in this protein, which is nervous. The new study showed that this part plays an important role in maintaining the elasticity of protein, which helps to form dynamic molecular gatherings, known as ‘molecular condensation’ and breaking it down. The nerve microxon is a very small part of the Oxon, which is the genetic pieces used to form a moral Rena (the Murse Ribosic DNA) during the genetic copy process. Unlike ordinary oxone, microxon is characterized by the small size, often consists only of a few nitrogen rules, but it plays a decisive role in regulating molecular functions of neurons. The researchers pointed out that the lack of this small part causes disturbance of molecular condensation, which is small meetings in the cells that store important molecules such as the messenger in an inactive state. This condensation collects and disintegrates in response to cellular signals, which enables dynamic regulation of genes. Without the microxon, condensation becomes less dynamic and forms solid groups, which impede the introduction of the stored Murtur. The disruption of genes that regulate this imbalance reduces the production of proteins needed for nerve growth and functions, which can contribute to the occurrence of autism symptoms. The study confirmed that the absence of microxon imbalances in regulating genes responsible for the development of the brain, leading to deviations from nervous growth that can be manifested as symptoms of autism. This discovery helps to explain the complex and diverse nature of unknown autism, which in cases includes a wide range of symptoms and severity. The researchers pointed out that the microxon can work briefly, which means that this small order can be placed in the cells to restore a partially CPEB4 function and reduce the symptoms. Although this approach is still in its exploratory stages, it is hope of developing purposeful treatments. The researchers said that the next step contains additional experiments on animal models; To ensure that these results can be applied in human treatments. The team hopes that this research will improve the quality of life for individuals and families affected by autism.