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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 SOD1^G93A/VEGF^+/+ double-transgenic mice show delayed motor neuron loss, delayed motor impairment, and prolonged survival compared with SOD1^G93A 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

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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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