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The Journal of Neuroscience, January 10, 2007, 27(2):304-307; doi:10.1523/JNEUROSCI.4433-06.2007
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Brief Communications
Vascular Endothelial Growth Factor Overexpression Delays Neurodegeneration and Prolongs Survival in Amyotrophic Lateral Sclerosis Mice
Yaoming Wang,1
Xiao Ou Mao,1
Lin Xie,1
Surita Banwait,1
Hugo H. Marti,2
David A. Greenberg,1 and
Kunlin Jin1
1Buck Institute for Age Research, Novato, California 94945, and 2Institute of Physiology and Pathophysiology, University of Heidelberg, D-69117 Heidelberg, Germany
Correspondence should be addressed to Kunlin Jin, Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945. Email: kjin{at}buckinstitute.org
We sought genetic evidence for the involvement of neuronal vascular endothelial growth factor (VEGF) in amyotrophic lateral sclerosis (ALS). Mice expressing human ALS mutant superoxide dismutase-1 (SOD1) were crossed with mice that overexpress VEGF in neurons (VEGF+/+). We report that SOD1G93A/VEGF+/+ double-transgenic mice show delayed motor neuron loss, delayed motor impairment, and prolonged survival compared with SOD1G93A single transgenics. These findings indicate that neuronal VEGF protects against motor neuron degeneration, and may have therapeutic implications for ALS.
Key words: vascular endothelial growth factor; amyotrophic lateral sclerosis; motor neuron; superoxide dismutase-1; transgenic; neurodegeneration
Received July 18, 2006;
revised Nov. 23, 2006;
accepted Nov. 26, 2006.
Correspondence should be addressed to Kunlin Jin, Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945. Email: kjin{at}buckinstitute.org
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