Prenatal exposure to infectious or inflammatory insults is increasingly recognized to play an important role in the etiology neurodevelopmental disorders, such as schizophrenia, autism and bipolar disorder. The molecular processes underlying this pathological association, however, are only partially understood, and the majority of the experimental attempts to answer this question are hypothesis-driven investigations that may mask the discovery of novel disease mechanisms. Using a well-established mouse model of prenatal viral-like immune activation, Juliet Richetto and collaborators demonstrate, with a multi-system unbiased approach, that prenatal viral-like immune activation causes myelin-related transcriptional and epigenetic changes in corticostriatal areas.
These findings, recently published in Cerebral Cortex, may provide a molecular mechanism whereby prenatal infection can impair myelin functionality and stability, ultimately concurring to the brain and behavioral alterations observed in neurodevelopmental diseases.
Please use the following link to access the article published in Cerebral Cortex: