The findings indicate that the amygdala’s critical period plasticity is elevated and may shift to earlier developmental times. This could cause a ‘maladaptive’ type of pliancy but one that can be treated with helpful mediation at key formative time focuses.
A recent study suggests that therapeutic interventions to treat neurodevelopmental disorders may be more effective if they are carried out at the very beginning of the brain’s development.
“It is essential to determine how and when brain circuits change during development in order to stop the progression of neurodevelopmental disorders. Molly Huntsman, PhD, senior author of the study and associate professor at the University of Colorado Skaggs School of Pharmacy and Pharmaceutical Sciences on the University of Colorado Anschutz Medical Campus, stated, “Our study identifies when circuits are altered in addition to how brain circuits are corrected.”
A common cause of intellectual disability, autism, and anxiety disorders, Fragile X Syndrome (FXS) is the subject of the study, which was recently published in The Journal of Neuroscience.
“We’re hoping to provide answers for when and how to treat FXS to help with therapeutic options eventually,” Huntsman stated. “Currently, there are no approved or effective therapies targeting specific pathophysiology underlying the clinical manifestations of FXS.”
During a crucial stage of brain development that is susceptible to therapeutic intervention, the researchers from the CU Skaggs School of Pharmacy discovered potential causal changes at the circuit level. They focused on the amygdala, the part of the brain that processes fear and anxiety.
Overview
They discovered a crucial period of increased circuit plasticity in the early stages of brain development by employing a mouse model of FXS. They demonstrated that during these periods of increased plasticity, fear-learning emerges in the brain. They also demonstrated that early intervention improves it.
The findings indicate that the amygdala’s critical period plasticity is elevated and may shift to earlier developmental times. This could cause a ‘maladaptive’ type of pliancy but one that can be treated with helpful mediation at key formative time focuses.
According to the study, age at treatment is important because early pharmacological intervention reduced fear-learning in the mouse model.
According to Huntsman, “This is extremely significant and addresses a critical barrier for understanding how circuits develop in a mouse model of autism and intellectual disability, and even more important, for therapeutic intervention-directed treatment options.”
