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Brain Advance Access originally published online on December 9, 2005
Brain 2006 129(2):480-489; 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@oupjournals.org

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

Anna-Leena Sirén1,4, Konstantin Radyushkin1,2, Susann Boretius3, Daniel Kämmer1, Claas-Christian Riechers1, Oliver Natt3, Derya Sargin1, Takashi Watanabe3, Swetlana Sperling1, Thomas Michaelis3, Jack Price5, Barbara Meyer2, Jens Frahm3 and Hannelore Ehrenreich1

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

Correspondence to: Prof. Hannelore Ehrenreich, MD, DVM, Division of Clinical Neuroscience, Max Planck Institute of Experimental Medicine, Hermann-Rein Strasse 3, 37075 Göttingen, Germany E-mail: ehrenreich{at}em.mpg.de

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.

Key Words: EPO; MRI; neuroprotection; neurodegeneration; neurotrauma; schizophrenia

Abbreviations: BBB = blood-brain barrier; BrdU = bromodeoxyuridine; EPO = erythropoietin

Received July 1, 2005. Revised September 26, 2005. Accepted October 27, 2005.


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