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Neurology Research International
Volume 2012, Article ID 295389, 17 pages
Review Article

Modeling the Encephalopathy of Prematurity in Animals: The Important Role of Translational Research

1Department of Pathology, Children’s Hospital Boston and Harvard Medical School, Boston, MA 02115, USA
2Department of Neurology, Children’s Hospital Boston and Harvard Medical School, Boston, MA 02115, USA

Received 29 November 2011; Accepted 18 January 2012

Academic Editor: Tara DeSilva

Copyright © 2012 Hannah C. Kinney and Joseph J. Volpe. 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.


Translational research in preterm brain injury depends upon the delineation of the human neuropathology in order that animal models faithfully reiterate it, thereby ensuring direct relevance to the human condition. The major substrate of human preterm brain injury is the encephalopathy of prematurity that is characterized by gray and white matter lesions reflecting combined acquired insults, altered developmental trajectories, and reparative phenomena. Here we highlight the key features of human preterm brain development and the encephalopathy of prematurity that are critical for modeling in animals. The complete mimicry of the complex human neuropathology is difficult in animal models. Many models focus upon mechanisms related to a specific feature, for example, loss of premyelinating oligodendrocytes in the cerebral white matter. Nevertheless, animal models that simultaneously address oligodendrocyte, neuronal, and axonal injury carry the potential to decipher shared mechanisms and synergistic treatments to ameliorate the global consequences of the encephalopathy of prematurity.