Experiment with rodents showed the role of HNRNP A1 in maintaining the myelin sheath, a layer that protects the extensions of neurons
Research on Journal of Neurochemistry Detaled the role of a protein, HNRNP A1, in myelin formation and stability, suggesting an important impact on neurodegenerative diseases and mental disorders such as multiple sclerosis and schizophrenia. The findings open the way for further research and potential treatments.
Myelin is a greasy substance, produced by oligodendrocytes (central nervous system cells), which forms a sheath, as a kind of “insulating” that “protects” neuron extensions (axons) and increases the velocity of nerve impulses that transmit information between neural cells. In the scientific literature, patients with multiple sclerosis and schizophrenia lose myelin (so -called demyelinization), leaving part of the axons “unleashed” and causing damage to brain functions.
The study, done in rodents, investigated changes in essential proteins for myelin production (myelinization). And the results highlight the involvement of HNRNP A1 in maintaining the integrity of this protective sheath.
HNRNP A1 regulates the processing of messenger RNA, ie adjusts how the molecule is cut and assembled (splicing), determining which proteins will be produced and in which quantities. Studied for years by this group of scientists from Unicamp (State University of Campinas), HNRNP A1 had already appeared prominent in previous research made with brain tissue of people with schizophrenia and cells cultivated in laboratories.
“When I was in the master’s degree, I worked with oligodendrocyte predecessor cell lineages and their antipsychotics responses. This protein, HNRNP A1, always appeared. We decided to try to understand its role in oligodendrocytes. But it was necessary to use an animal model to induce myelinization and understand the process.”said, 1st Author of the article and doctorate from FAPESP at the Unicamp Institute of Biology.
For the researcher, also from IB-Unicamp and corresponding author of the work, myelin has been an important target of study for neuropsychiatric diseases.
“We were able to analyze the process of demyelinization in animals and then restore the myelin sheath. This allowed an interesting study window. We did behavioral tests to evaluate locomotion, short and long -term memory and social interaction. When myelin is restored, all these functions return to the brain.”said Crinfli, who was FAPESP scholarship in.
Teles mentions that this was one of the results that caught the group’s attention – the fact that the changes were detected at the molecular level, without affecting, however, the behavior of animals.
“With this molecular and non-behavioral change, work has an interesting potential to point out an important protein in the establishment of schizophrenia. This same animal model is analyzed in research for multiple sclerosis, for example, and when behavioral study there is changes. In the case of schizophrenia, the fact that behavior is not changed points out, in my assessment, that this protein is essential in the development of the disease, and may have an influence on its genesis.”declared the teacher, from IB-Unicamp, advisor of Teles and responsible for the.
Schizophrenia is a mental disorder characterized by the loss of contact with reality (psychosis), hallucinations, delusions and worseness of cognition, among others. The exact cause is still unknown, but recent research suggests a combination of hereditary factors, with molecular and functional changes in the brain. Treatment is performed with antipsychotic medicines and psychotherapy.
It is estimated that in Brazil about 1.6 million people have schizophrenia. In the world, the prevalence is approximately 1% of the world’s population.
For years, Martins-de-Souza’s research group has been working to understand the role of oligodendrocytes in schizophrenia, having managed to map a series of brain proteins that help unravel the molecular bases of the disorder (read more).
To understand the research
The group adopted a rodent model (Murino) that has also been studied in cases of multiple sclerosis, a disease characterized by severe demyelinization.
From the 8th week of the experiment was induced to demyelinization, which lasted another 5 weeks. Then the process was interrupted and the myelin sheath was restored. During this period, the researchers analyzed the activity of HNRNP A1. “We saw that myelin -related proteins in these animals were all diminished. Disturbing the activity of this protein [hnRNP A1]we ended up disrupting myelinization ”said Teles.
For scientists, exploring the impacts of protein changes on synaptic transmission and cognitive processes can reveal new therapeutic targets.
In addition to the scholarships, the research also received support from FAPESP through 6 other projects (,,,).
The article Impacts of hnRNP A1 Splicing Inhibition on the Brain Remyelination Proteome can be read.
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