Journal Article

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

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

in Brain

Published on behalf of The Guarantors of Brain

Volume 129, issue 2, pages 480-489
Published in print February 2006 | ISSN: 0006-8950
Published online December 2005 | e-ISSN: 1460-2156 | DOI: http://dx.doi.org/10.1093/brain/awh703
Global brain atrophy after unilateral parietal lesion and its prevention by erythropoietin

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

Journal Article.  6414 words.  Illustrated.

Subjects: Neurology ; Neuroscience

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