Kinney Hannah C, Volpe Joseph J
Department of Pathology, Children's Hospital Boston and Harvard Medical School, Boston, MA 02115, USA.
Neurol Res Int. 2012;2012:295389. doi: 10.1155/2012/295389. Epub 2012 May 23.
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.
早产脑损伤的转化研究依赖于对人类神经病理学的描绘，以便动物模型能够忠实地重现它，从而确保与人类状况直接相关。人类早产脑损伤的主要基质是早产儿脑病，其特征是灰质和白质病变，反映了后天性损伤、发育轨迹改变和修复现象的综合作用。在这里，我们强调了人类早产脑发育和早产儿脑病的关键特征，这些特征对于动物模型的构建至关重要。在动物模型中完全模拟复杂的人类神经病理学是困难的。许多模型关注与特定特征相关的机制，例如，脑白质中少突胶质前体细胞的丢失。然而，同时解决少突胶质细胞、神经元和轴突损伤的动物模型有可能破解共同机制和协同治疗方法，以改善早产儿脑病的整体后果。
