A Peptide Derived from Activity-Dependent Neuroprotective Protein (ADNP) Ameliorates Injury Response in Closed Head Injury in Mice

• Published in: The Journal of pharmacology and experimental therapeutics 2001-01, Vol.296 (1), p.57-63
• Main Authors: Beni-Adani, Liana, Gozes, Illana, Cohen, Yoram, Assaf, Yaniv, Steingart, Ruth A., Brenneman, Douglas E., Eizenberg, Oded, Trembolver, Victoria, Shohami, Esther
• Format: Article
• Language: English
• Subjects: Animals; Behavior, Animal - drug effects; Brain Edema - drug therapy; Brain Edema - pathology; Head Injuries, Closed - drug therapy; Head Injuries, Closed - mortality; Head Injuries, Closed - psychology; Homeodomain Proteins; Magnetic Resonance Imaging; Male; Mice; Mice, Inbred Strains; Nerve Tissue Proteins - metabolism; Nerve Tissue Proteins - therapeutic use; Neuroprotective Agents - metabolism; Neuroprotective Agents - therapeutic use; PC12 Cells; Peptides - metabolism; Peptides - therapeutic use; Postural Balance - drug effects; Rats; Tumor Necrosis Factor-alpha - antagonists & inhibitors; Tumor Necrosis Factor-alpha - metabolism; Tumor Necrosis Factor-alpha - toxicity
• ISSN: 0022-3565; 1521-0103
• DOI: 10.1016/S0022-3565(24)29662-2

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.