title: NeuroAiD: properties for neuroprotection and neurorepair.
abstract: BACKGROUND
  Treatments for stroke and other brain injuries are limited. NeuroAiD has been shown to be beneficial in clinical studies. We reviewed the pharmacological effects of NeuroAiD on the normal and ischemic brain and neurons.
  
  
  METHODS
  In vivo and in vitro experiments using mouse model of stroke (focal ischemia), rat model of cardiac arrest (global ischemia) and cortical neurons in culture were reviewed and summarized.
  
  
  RESULTS
  NeuroAiD improved survival, attenuated infarct size, improved functional recovery in the model of focal ischemia, and protected neurons against glutamate-induced injury. Furthermore, it enhanced cognitive recovery by reducing hippocampal CA1 cell degeneration, DNA fragmentation, Bax expression and ma-londialdehyde release in the model of global ischemia. Activation of the Akt survival pathway and opening of KATP channels may contribute to the neuroprotective properties of NeuroAiD. NeuroAiD increased BDNF expression and induced proliferation of cells which differentiate and mature into neurons. It enhanced rosette formation of human embryonic stem cells. NeuroAiD-treated embryonic cortical neurons developed into neurons with longer neurites, denser outgrowths and networks, and more synaptic release sites.
  
  
  CONCLUSIONS
  NeuroAiD demonstrated both neuroprotective and neuroregenerative properties in rodent models of focal and global ischemia and in cortical cell cultures. These properties would be important for developing a treatment strategy in reducing the long-term disability of stroke, cardiac arrest and other brain injuries.
authors.affiliation: Institut de Pharmacologie Moléculaire et Cellulaire, Centre National de la Recherche Scientifique (CNRS), Université Nice Sophia Antipolis, Valbonne, France.
authors.forename: C
authors.initials: C
authors.lastname: Heurteaux
authors.forename: C
authors.initials: C
authors.lastname: Widmann
authors.forename: H
authors.initials: H
authors.lastname: Moha ou Maati
authors.forename: H
authors.initials: H
authors.lastname: Quintard
authors.forename: C
authors.initials: C
authors.lastname: Gandin
authors.forename: M
authors.initials: M
authors.lastname: Borsotto
authors.forename: J
authors.initials: J
authors.lastname: Veyssiere
authors.forename: B
authors.initials: B
authors.lastname: Onteniente
authors.forename: M
authors.initials: M
authors.lastname: Lazdunski
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology; D001923:Brain Chemistry / Q000187:drug effects; D001930:Brain Injuries / Q000188:drug therapy*; D002545:Brain Ischemia / Q000188:drug therapy; D004365:Drugs, Chinese Herbal / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D051379:Mice; D009416:Nerve Regeneration / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D020521:Stroke / Q000188:drug therapy*
chemical_list: D004365:Drugs, Chinese Herbal; C546417:Neuroaid; D018696:Neuroprotective Agents