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Brain Advance Access published online on December 9, 2005
Brain, doi:10.1093/brain/awh703
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© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received July 1, 2005
Revised September 26, 2005
Accepted October 27, 2005

Article

Global brain atrophy after unilateral parietal lesion and its prevention by erythropoietin

Anna-Leena Sirén 1, Konstantin Radyushkin 2, Susann Boretius 3, Daniel Kämmer 4, Claas-Christian Riechers 4, Oliver Natt 3, Derya Sargin 4, Takashi Watanabe 3, Swetlana Sperling 4, Thomas Michaelis 3, Jack Price 5, Barbara Meyer 6, Jens Frahm 3, and Hannelore Ehrenreich 4 *

1 Division of Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany; Section of Experimental Neurosurgery, Department of Neurosurgery, University of Würzburg, Würzburg, Germany
2 Division of Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany; Department of Molecular Cell Biology, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany
3 Biomedizinische NMR Forschungs GmbH, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany
4 Division of Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Göttingen, Germany
5 Institute of Psychiatry, King's College London, London, UK
6 Department of Molecular Cell Biology, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany

* To whom correspondence should be addressed.
Hannelore Ehrenreich, E-mail: ehrenreich{at}em.mpg.de


  Abstract

In humans, neurotrauma is suspected to cause brain atrophy and accelerate slowly progressive neurodegenerative disorders, such as Alzheimer's disease or schizophrenia. However, a direct link between brain injury and subsequent delayed global neurodegeneration has remained elusive. Here we show that juvenile (4-week-old) mice that are given a discrete unilateral lesion of the parietal cortex, develop to adulthood without obvious clinical symptoms. However, when monitored 3 and 9 months after lesioning, using high-resolution three-dimensional MRI and behavioural testing, the same mice display global neurodegenerative changes. Surprisingly, erythropoietin, a haematopoietic growth factor with potent neuroprotective activity, prevents behavioural abnormalities, cognitive dysfunction and brain atrophy when given for 2 weeks after acute brain injury. This demonstrates that a localized brain lesion is a primary cause of delayed global neurodegeneration that can be efficiently counteracted by neuroprotection.

Keywords: EPO; MRI; neuroprotection; neurodegeneration; neurotrauma; schizophrenia.
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