Autism genes can be rotated by a special trigger

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Despite the many promising results of studies in the relationship of autism, this spectrum of the disease is still poorly understood and difficult to correct or treat. However, a talented team of specialists from the University of Toronto today presented the results of their new study on the analysis of the functioning and role of a particular protein compound under the CPEB4 index, which they believe is the responsible agent for the development and distribution of certain genes related in one way or another to symptoms and features autism in terms of neuroplasty and neurobiology.

It is worth noting that earlier other teams of specialists found certain relationships between the work of certain genes and the symptoms of autism, which indicates a theoretical possibility of alternating this relationship. So, Canadian neuroscientists have begun to study this possibility, having compiled something like a genomic map. After spending a lot of time researching the most promising candidates that violate somatic processes and functions, they found that it was a protein called CPEB4 that is responsible for the dysfunction of some genes. In addition, this protein compound directly affects neuroplasticity and changes in various parts of the brain from the point of view of neurochemistry.

They also conducted preliminary studies on mice, which, using genetic engineering, disabled the functionality of this protein – as a result, changes in the brain began to occur associated with changes in gene production, which was expressed in the autistic behavior of mice.

Thus, experts were able to more or less clearly establish the relationship between individual types of genes and autism symptoms – however, using the modern genetic engineering complex. The presented protein compound, according to scientists, is subject not only to study, but also to the possibility of change – in order to, in turn, change the production of certain genes associated with the onset and development of autism.

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