In epilepsy, BAD is not really bad.
In this issue of Neuron, Giménez-Cassina et al. (2012) show that fuel utilization by neuronal mitochondria, controlled by the Bcl-2 family member BAD, defines response to seizures. Control of K(ATP) channels by mitochondrial metabolism might be a target for antiepileptic therapies.
Department of Cell Physiology and Medicine, University of Geneva, 1 Rue M. Servet, 1205 Geneve, Switzerland.
Elena
E
Ziviani
Luca
L
Scorrano