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

MPG-Autoren
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Sirén,  Anna-Leena
Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Radyushkin,  Konstantin
Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Kämmer,  Daniel
Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Riechers,  Claas-Christian
Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Sargin,  Derya
Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Sperling,  Swetlana
Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Ehrenreich,  Hannelore
Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society;

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Zitation

Sirén, A.-L., Radyushkin, K., Boretius, S., Kämmer, D., Riechers, C.-C., Natt, O., et al. (2006). Global brain atrophy after unilateral parietal lesion and its prevention by erythropoietin. Brain, 129, 480-489. doi:10.1093/brain/awh703.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-002A-23D6-5
Zusammenfassung
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.