Vascular Endothelial Growth Factor Overexpression Delays Neurodegeneration and Prolongs Survival in Amyotrophic Lateral Sclerosis Mice

• Published in: The Journal of neuroscience Vol. 27; no. 2; pp. 304 - 307
• Main Authors: Wang, Yaoming, Ou Mao, Xiao, Xie, Lin, Banwait, Surita, Marti, Hugo H, Greenberg, David A, Jin, Kunlin
• Format: Journal Article
• Language: English
• Published: United States Soc Neuroscience 10.01.2007; Society for Neuroscience
• Subjects: Amyotrophic Lateral Sclerosis - metabolism; Amyotrophic Lateral Sclerosis - mortality; Amyotrophic Lateral Sclerosis - pathology; Animals; Brief Communications; Disease Models, Animal; Gene Expression Regulation - physiology; Gene Expression Regulation, Enzymologic - physiology; Humans; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Motor Neurons - pathology; Nerve Degeneration - enzymology; Nerve Degeneration - metabolism; Nerve Degeneration - pathology; Nerve Degeneration - prevention & control; Superoxide Dismutase - biosynthesis; Superoxide Dismutase - genetics; Superoxide Dismutase-1; Survival Rate; Vascular Endothelial Growth Factor A - biosynthesis; Vascular Endothelial Growth Factor A - genetics; Vascular Endothelial Growth Factor A - physiology
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/JNEUROSCI.4433-06.2007

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.