Scientists from the University of North Carolina School of Medicine discovered the molecule microRNA-29 described as a powerful controller of mammal brain maturation. Removing microRNA from mice led to problems similar to epilepsy, autism, and a host of other neurodevelopmental disorders.
Study findings show a significant process in the brain's normal maturation as it identifies the likelihood that disrupting the process may result in multiple brain diseases.
MicroRNA-29 Identified as Common in Neurodevelopmental Disorders
Researchers revealed that abnormalities in microRNA-29 activity had been identified as a "common theme" in neurodevelopmental conditions and other behavioral differences among individuals. The study suggests boosting microRNA-29 levels and perhaps delivering the molecule directly would eventually become therapeutic options for individuals suffering from neurodevelopmental conditions, such as autism.
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MicroRNAs (MiR) consists of short ribonucleic acid stretches within cells that control gene expression. Each microRNA can bind to an RNA transcript from other genes, avoiding translation into protein. MiRNAs assume their role as inhibitors of gene activity, and the typical microRNA controls multiple genes to prevent genetic information from being overexpressed. These essential controllers have been extensively researched only in the last two decades. Thus, their roles in health and disease are yet to be discovered.
Researchers aimed to discover microRNAs part of the brain's maturation after birth, a human phase that consists of about the first 20 years of life. When they searched for the microRNAs that are more active in the adult mouse brain than the young mouse brain, a set of mRNA stood out from the rest. They found out that levels of the miR-29 family were 50 to 70 times higher in the adult mouse brain than in the young mouse brains.
Developing Problematic Disorders
The scientists studied a mouse model and removed the miR-29 family of genes in the brain. They say that while the mice were normally born, they developed a host of problems, such as repetitive behaviors, hyperactivity, and other abnormal traits normally observed in autistic mice and other neurodevelopmental conditions. A number of these mice developed epileptic seizures.
Researchers also sought out the cause of these abnormalities, examining gene activity in the mice's brains, comparing them to activity in mice that had miR-29. They found out that genes were more active when miR-29 was no longer present to block that activity. The scientists, however, found a large set of genes, which are associated with brain cells that were less active without miR-29.
Reason Behind Reduction in Gene Activity
Scientists then discovered what was behind the decrease in gene activity.
A target gene that miR-29 normally blocks encodes for the enzyme DNMT3A. The enzyme brings special chemical modifications called CH-methylations to DNA, silencing the genes inactivity.
To validate DNMT3A's role, scientists developed a distinctive mouse model that prevents miR-29 from hindering DNMT3A but leaving other targets of miR-29 untouched. Unleashing DNMT3A on its own leads to many of the same health problems, such as seizures and even death, as evident in the mice without miR-29.
The results show a crucial process in molding the brain late in its development, which is turning off DNMT3A to free up active genes in the brain.
Researchers are currently studying how the absence of miR-29 would lead to neurodevelopmental conditions and discovering how the miR-29's activity is controlled in childhood to improve brain functions, giving humans the traits that make them unique individuals.
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