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Neurology Research International
Volume 2012, Article ID 506320, 16 pages
http://dx.doi.org/10.1155/2012/506320
Review Article

Molecular Mechanisms of Neonatal Brain Injury

1Centre for the Developing Brain, Institute of Reproductive and Developmental Biology, Department of Surgery and Cancer, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
2Perinatal Center, Institutes of Clinical Sciences & Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, 405 30 Gothenburg, Sweden
3Inserm, U676, 75019 Paris, France
4Faculté de Médecine, Université Paris Diderot, 75013 Paris, France

Received 3 October 2011; Accepted 11 October 2011

Academic Editor: Jianrong Li

Copyright © 2012 Claire Thornton et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Fetal/neonatal brain injury is an important cause of neurological disability. Hypoxia-ischemia and excitotoxicity are considered important insults, and, in spite of their acute nature, brain injury develops over a protracted time period during the primary, secondary, and tertiary phases. The concept that most of the injury develops with a delay after the insult makes it possible to provide effective neuroprotective treatment after the insult. Indeed, hypothermia applied within 6 hours after birth in neonatal encephalopathy reduces neurological disability in clinical trials. In order to develop the next generation of treatment, we need to know more about the pathophysiological mechanism during the secondary and tertiary phases of injury. We review some of the critical molecular events related to mitochondrial dysfunction and apoptosis during the secondary phase and report some recent evidence that intervention may be feasible also days-weeks after the insult.