A peptide derived from Activity-Dependent Neuroprotective Protein (ADNP) ameliorates injury response in closed head injury in mice

Abstract

Brain injury induces disruption of the blood-brain barrier, edema, and release of autodestructive factors that produce delayed neuronal damage. NAPSVIPQ (NAP), a femtomolar-acting peptide, is shown to be neuroprotective in a mouse model of closed head injury. NAP injection after injury reduced mortality and facilitated neurobehavioral recovery (P < 0.005). Edema was reduced by 70% in the NAP-treated mice (P < 0.01). Furthermore, in vivo magnetic resonance imaging demonstrated significant brain-tissue recovery in the NAP-treated animals. NAP treatment decreased tumor necrosis factor-α levels in the injured brain and was shown to protect pheochromocytoma (PC12 cells) against tumor necrosis factor-α-induced toxicity. Thus, NAP provides significant amelioration from the complex array of injuries elicited by head trauma

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