Not sure if nbritton is still around or not but after skimming some of the links he provided previously it looks like it addresses the NMDA hypofunction issue. So for sz there are 2 major theories one involves dopamine and one involves glutamate which binds to and activates the NMDA receptor. They are interlinked in a few ways for example dopamine signalling through the D2 receptor decreases baseline NMDA function so this may be one way the APs affect the NMDA pathway. NMDA fuctioning too low can be mimicked by the street drugs PCP and ketamine. So the way pregnenolone works is to increase the number of NMDA receptors on the cell surface so you end up getting more signal with the same amount of glutamate so theoretically it relieves the hypofunction. The one thing I would warn you about is that too much NMDA activity is actually neurotoxic so its a very delicate balance. This is one of the reasons we don't have any prescribed drugs targeting this protein yet. They are working on something that will regulate the glycine modulatory site as a treatment for sz rather than targeting the glutamate binding directly.