According to previous studies the phenotype of offspring in this mouse model is highly variable, but reminiscent of human FAS with growth restriction, similar structural changes to corresponding areas of the face and skull, and hyperactivity. In this study we wanted to determine the impact of alcohol on the structures of the central nervous system.
We observed that early exposure to alcohol caused subtle changes in the epigenome and altered the function of several genes in the hippocampi of adolescent mice. We also detected alcohol-induced alterations in the brain structure of adult offspring. Interestingly, we also found out that in addition to hippocampus, alcohol caused similar changes to gene function in two different tissues of the infant mouse, bone marrow and the olfactory epithelium of the snout. These results support our hypothesis that early gestational ethanol exposure alters the epigenetic reprogramming of the embryo, which leads to alterations in gene regulation and embryonic development, and causes life-long changes in brain structure, function, and behaviour.
Our results suggest that alcohol-induced changes in embryonic development can occur in very early stage of pregnancy. Therefore it would be good to decrease the alcohol consumption as soon as pregnancy is planned. It is also important to remember, that this is a mouse, not a human study. We cannot directly compare our findings in this mouse model to human.
Next we will focus on the asymmetry of brain structures, especially alcohol-induced alterations in hippocampus. In addition to the mouse studies we are collecting human samples in a project called epiFASD. We hope that in the future both mouse model and human samples will help us understand the molecular mechanisms of gestational ethanol exposure.