Newly Identified Pathway Links Fetal Brain Development to Adult Social Behavior; Intervention in Mouse Model Prevents Aberrant Behavior in Adult; Findings May Be Relevant to Autism

Fetal development has been known to play an important role in social interaction, a fundamental behavior found in nearly all organisms, and later adult social behaviors. Autism, a highly heritable neurodevelopment disorder that causes difficulties with social interactions, has been postulated to be caused by neuron overgrowth in the prenatal period, although the precise timing and cause of this overgrowth has been unknown. Recently, researchers at the Case Western Reserve University School of Medicine, the University of California at San Francisco (UCSF) School of Medicine, and other institutions have uncovered abnormalities in embryonic brain development in mice, including transient embryonic brain enlargement during neuron formation, that are responsible for abnormal adult brain structures and behavioral abnormalities in adult mice. These findings demonstrate a fetal origin for social and repetitive behavior deficits, as seen in disorders such as autism. Using engineered mice, the researchers identified a critical period during embryonic brain development for the establishment of normal social behavior and they were able to link this critical period with abnormalities in specific adult brain structures. After identifying these abnormalities, the researchers were then able to intervene and treat mice during fetal development. The embryonically treated mice progressed without adult behavioral deficits. Further studies will be required to determine the consequences of abnormal development of cortical neurons on adult brain circuitry and function, as well as possible therapeutic interventions. The results of the study were published online on February 2, 2014 in Molecular Psychiatry. The article is titled “Prenatal β-catenin/Brn2/Tbr2 Transcriptional Cascade Regulates Adult Social and Stereotypic Behaviors.”
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