Vascular Endothelial Growth Factor Overexpression Delays Neurodegeneration and Prolongs Survival in Amyotrophic Lateral Sclerosis Mice
- Yaoming Wang1,
- Xiao Ou Mao1,
- Lin Xie1,
- Surita Banwait1,
- Hugo H. Marti2,
- David A. Greenberg1, 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. kjin{at}buckinstitute.org
Abstract
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.
- vascular endothelial growth factor
- amyotrophic lateral sclerosis
- motor neuron
- superoxide dismutase-1
- transgenic
- neurodegeneration
- Copyright © 2007 Society for Neuroscience 0270-6474/07/270304-04$15.00/0
