The Neurulation Biomechanics (Galea) Lab aims to improve prediction, prevention and patient outcomes for those affected by neural tube defects such as spina bifida. Our research relies on three key experimental systems: animal models of human congenital malformations, patient-derived tissues, and human induced pluripotent stem cells. We strive to bridge the gap in our understanding between genetic/molecular mechanisms and their tissue-level consequences which underlie congenital malformations. By combining different experimental systems, our research ranges from fundamental studies of key cellular behaviours to translational work aiming to improve outcomes for individuals who have spina bifida.

Our recently-published article shows that regional deletion of Fgfr1 in the embryonic trunk produces localised spinal mis-patterning and a terminal myelocystocele-like phenotype in mice. The image below shows a normal mouse fetus (left) and one with a sac-like protrusion at the bottom of the spinal cord (right) which resembles a rare human malformation called Terminal Myelocystocele. Our paper shows that this malformation does not arise because of failed neural tube closure, like more common types of spina bifida do, but happens are the neural tube is fully closed.