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Global brain atrophy after unilateral parietal lesion and its prevention by erythropoietin
Sirén, A.-L. ; Radyushkin, K.; Boretius, S. ; Kämmer, D. ; Riechers, C.-C. ; Natt, O. & Sargin, D. et al. (2006)
Brain, 129(2) pp. 480-489. DOI: https://doi.org/10.1093/brain/awh703 10.1093/brain/awh703
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- Sirén, Anna-Leena ; Radyushkin, Konstantin; Boretius, Susann ; Kämmer, Daniel ; Riechers, Claas-Christian ; Natt, Oliver ; Sargin, Derya ; Watanabe, Takashi ; Sperling, Swetlana ; Michaelis, Thomas ; Price, Jack; Meyer, Barbara ; Frahm, Jens ; Ehrenreich, Hannelore
- 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.
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