Iduna protects the brain from glutamate excitotoxicity and stroke by interfering with poly(ADP-ribose) polymer-induced cell death

Ischemia-perfusion injury and high doses of glutamate activate poly(ADP-ribose) (PAR) polymerase-1, leading to PAR polymer synthesis and cell death. Valina Dawson and her colleagues identify Iduna, an endogenous inhibitor of PAR polymer–induced cell death. Iduna is induced with low-dose NMDA receptor activation, binds PAR polymer and protects against cell death both in vitro and in in vivo models of stroke.