CONSEQUENCES OF TRISOMY-16 FOR MOUSE-BRAIN DEVELOPMENT - CORTICOGENESIS IN A MODEL OF DOWN-SYNDROME

We have studied abnormalities in the tangential and radial expansion o f the cerebral cortex during fetal development in the trisomy 16 (Ts16 ) mouse, a model for human trisomy 21 (Down syndrome). Slowed tangenti al expansion of the neuroepithelium in Ts16 resulted in a reduction of final telencephalic size and is predicted to decrease the number of r adial cortical units in the mature brain. In addition, radial growth o f the Ts16 cortex was delayed at the time of peak cortical neurogenesi s in normal mice, but by embryonic day 18 the cortex reached normal th ickness. Because mouse chromosome 16 shares many genes with human chro mosome 21, abnormalities in Ts16 brain development may parallel abnorm alities in trisomy 21.