VEGF: necessary to prevent motoneuron degeneration, sufficient to treat ALS?
Since Charcot recognized the devastating disorder amyotrophic lateral sclerosis (ALS) in 1874, many theories have been proposed to explain its pathogenesis, but it remains as deadly and incurable as ever. Three years ago it was reported that reduced levels of vascular endothelial growth factor (VEGF) caused ALS-like motoneuron degeneration in mice. Recent evidence indicates that insufficient VEGF is also a risk factor for ALS in humans. Although VEGF was once considered to be only a specific angiogenic factor, emerging evidence indicates that it also displays important neuroprotective activity. These insights have primed widespread interest in developing VEGF-based therapies for (moto)neuron degenerative disorders, raising new hope for the treatment of ALS and other neurodegenerative diseases.
Lambrechts
Diether
D
The Center for Transgene Technology and Gene Therapy, Flanders Interuniversity Institute for Biotechnology, Katholieke Universiteit Leuven, B-3000 Leuven, Belgium.
Storkebaum
Erik
E
Carmeliet
Peter
P
D000690:Amyotrophic Lateral Sclerosis / Q000209:etiology* / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D000818:Animals; D004195:Disease Models, Animal; D020022:Genetic Predisposition to Disease; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D009046:Motor Neurons / Q000378:metabolism / Q000473:pathology*; D018696:Neuroprotective Agents / Q000378:metabolism; D012307:Risk Factors; D042461:Vascular Endothelial Growth Factor A / Q000172:deficiency* / Q000235:genetics
D018696:Neuroprotective Agents; D042461:Vascular Endothelial Growth Factor A